Journal articles: 'Myocardial infarction Chemotherapy'

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LAW, H. "Chemotherapy-induced myocardial infarction." European Heart Journal 17, no. 6 (June 2, 1996): 966–67. http://dx.doi.org/10.1093/oxfordjournals.eurheartj.a014984.

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Bissett, D., and S. B. Kaye. "Myocardial infarction after chemotherapy for testicular teratoma." Annals of Oncology 4, no. 5 (May 1993): 432. http://dx.doi.org/10.1093/oxfordjournals.annonc.a058529.

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Bachmeyer, Claude, Hervé Joly, and Roland Jorest. "Early Myocardial Infarction during Chemotherapy for Testicular Cancer." Tumori Journal 86, no. 5 (September 2000): 428–30. http://dx.doi.org/10.1177/030089160008600513.

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A 36-year-old man with testicular cancer had an acute myocardial infarction during the first course of chemotherapy with bleomycin, etoposide and cisplatin. Since the patient had no significant risk factors for coronary heart disease, the infarction was likely to be attributable to the chemotherapy regimen. The physiopathological mechanisms of this causal relationship are discussed here.

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Kashiwagi, Yoshiyuki. "A Case of Acute Myocardial Infarction during Chemotherapy of Advanced Rectal Cancer." Nurse Media Journal of Nursing 8, no. 2 (March 4, 2019): 96. http://dx.doi.org/10.14710/nmjn.v8i2.18908.

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Background:Cetuximab and irinotecan, levoforinate, 5-FU (FOLFIRI) are administered to advanced colorectal cancer. Although this regimen is standardized for recurrent metastatic colorectal cancer, the merger of myocardial infarction is rare.Purpose:The aim of this study is consider factors of myocardial infarction that developed during chemotherapy of colorectal cancer.Method:We conduct a retrospective study of cases in which myocardial infarction develops during chemotherapy in colorectal cancer on the basis of medical records, nursing records and physiological function test results.Case:A 80-year-old man was in chemotherapy with cetuximab + FOLFIRI in outpatient with multiple lung metastasis diagnosis after rectal cancer surgery.Result:Three days after the 38th administration, the patient visited an emergency outpatient mainly with complaints of dyspnea and back pain. Electrocardiogram was a finding that the lower wall infarction is suspected. The patient of bi-aspirin oral administration and chest pain 10 mg of morphine hydrochloride was injected via intravenous drip infusion, and it was transferred to a specialized cardiovascular hospital.Emergency coronary angiography was performed in the diagnosis of acute myocardial infarction, and percutaneous coronary intervention was performed because the left anterior descending branch complete occlusion was recognized. After thrombus aspiration, the balloon was dilated, the stent was placed, and reperfusion was successfully completed. The patient was discharged on the 10th disease day.In this case, it is thought that cetuximab + FOLFIRI synergistically induced hyperthrombogenicity, coronary plaque erosion, and acute myocardial infarction.It may also be necessary for interventions such as monitoring of risks in daily living by the medical care provider and guidance on risk avoidance behaviors.brief background of the topic and significance of the study.Conclusion:In this case, it is thought that cetuximab + FOLFIRI synergistically induced hyperthrombogenicity, coronary plaque erosion, and acute myocardial infarction. It may also be necessary for interventions such as monitoring of risks in daily living by the medical care provider and guidance on risk avoidance behaviors.

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Ozben, Beste, Ramazan Kurt, Huseyin Oflaz, Murat Sezer, Mert Basaran, Taner Goren, and Sabahattin Umman. "Acute Anterior Myocardial Infarction After Chemotherapy for Testicular Seminoma in a Young Patient." Clinical and Applied Thrombosis/Hemostasis 13, no. 4 (October 2007): 439–42. http://dx.doi.org/10.1177/1076029607303334.

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Testicular cancer is the most common solid tumor among young men aged 15 to 35 years. Combination chemotherapy with cisplatin, etoposide, and bleomycin remains the mainstay of treatment. We present a 27-year-old man who presented with an acute anterior myocardial infarction during the second course of chemotherapy for seminoma. Because the patient had no significant risk factors for coronary heart disease, the infarction was likely caused by the chemotherapy regimen.

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Roy, Ambuj, Naveen Khanna, and Nagendra Boopathy Senguttuvan. "Rituximab-Vincristine Chemotherapy-Induced Acute Anterior Wall Myocardial Infarction with Cardiogenic Shock." Texas Heart Institute Journal 41, no. 1 (February 1, 2014): 80–82. http://dx.doi.org/10.14503/thij-12-2853.

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We present a case of an elderly man with coronary artery disease who was diagnosed with non-Hodgkin lymphoma. Soon after the administration of chemotherapy, which included rituximab and vincristine, he developed acute myocardial infarction with cardiogenic shock. The condition was managed successfully with primary percutaneous coronary intervention. We briefly discuss the possible pathogenic mechanisms of chemotherapy-induced ischemic syndrome and the management of chemotherapy in patients with high cardiovascular risk.

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House, Kenneth W., Sheryl R. Simon, and Reginald P. Pugh. "Chemotherapy-induced myocardial infarction in a young man with hodgkin's disease." Clinical Cardiology 15, no. 2 (February 1992): 122–25. http://dx.doi.org/10.1002/clc.4960150214.

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Bilir, Cemil, Hüseyin Engin, Yasemin Bakkal Temi, Bilal Toka, and Turgut Karabağ. "Acute Myocardial Infarction Caused by Filgrastim: A Case Report." Case Reports in Oncological Medicine 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/784128.

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Common uses of the granulocyte-colony stimulating factors in the clinical practice raise the concern about side effects of these agents. We presented a case report about an acute myocardial infarction with non-ST segment elevation during filgrastim administration. A 73-year-old man had squamous cell carcinoma of larynx with lung metastasis treated with the chemotherapy. Second day after the filgrastim, patient had a chest discomfort. An ECG was performed and showed an ST segment depression and negative T waves on inferior derivations. A coronary angiography had showed a critical lesion in right coronary arteria. This is the first study thats revealed that G-CSF can cause acute myocardial infarction in cancer patients without history of cardiac disease. Patients with chest discomfort and pain who are on treatment with G-CSF or GM-CSF must alert the physicians for acute coronary events.

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Alici, Hayri, Fethi Yavuz, Suleyman Ercan, and Vedat Davutoglu. "Chemotherapy related myocardial infarction in a young patient with yolk sac tumor." International Journal of the Cardiovascular Academy 1, no. 1 (June 2015): 21–23. http://dx.doi.org/10.1016/j.ijcac.2015.07.010.

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Dieckmann, K. P., A. Gerl, J. Witt, and J. T. Hartmann. "Myocardial infarction and other major vascular events during chemotherapy for testicular cancer." Annals of Oncology 21, no. 8 (August 2010): 1607–11. http://dx.doi.org/10.1093/annonc/mdp597.

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Thyagarajan, Braghadheeswar, Lubna Bashir Munshi, and Martin Miguel Amor. "Left Ventricular Aneurysm Presenting as a Late Complication of Childhood Chemotherapy." Case Reports in Cardiology 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/625451.

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Cardiotoxicity is a well known adverse effect of chemotherapy. Multiple cardiac injuries have been reported including cardiomyopathy, pericarditis, myocarditis, angina, arrhythmias, and myocardial infarction. A left ventricular aneurysm due to chemotherapy is a rare and a dangerous complication which is particularly challenging in diagnosis requiring a high index of suspicion and periodic imaging. We present a case of a young Caucasian male with a past medical history of Acute Lymphocytic Leukemia status after chemotherapy during his childhood diagnosed with left ventricular aneurysm several years later.

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Guskova, N. K., L. Yu Vladimirova, E. A. Sycheva, A. A. Morozova, D. A. Rosenko, A. K. Donskaya, O. N. Selyutina, A. M. Skopintsev, and N. V. Golomeeva. "Changes in the level of cardiomarkers in the development of acute myocardial infarction on the background of chemotherapy of a patient with tongue cancer." South Russian Journal of Cancer 2, no. 3 (September 8, 2021): 48–54. http://dx.doi.org/10.37748/10.37748/2686-9039-2021-2-3-6.

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Cancer is one of the leading causes of death and disability worldwide. Timely diagnosis and the introduction of new effective treatments, including intensive radiation and chemotherapy regimens, have significantly improved survival forecasts in recent years. At the same time, the use of these types of treatment increases the risk of complications, one of which includes chemotoxic cardiopathies. In this regard, timely detection and treatment of complications from the cardiovascular system in patients receiving chemotherapy courses in combination with surgical methods of treatment is important. This paper presents an assessment of the significance of the use of cardiomarkers in the early diagnosis of acute myocardial infarction that developed during chemotherapy in a patient with tongue cancer with a complicated cardiac history. Patient M., 45 years old, was admitted for surgical treatment for cancer of the tongue St. IVA, T4aN1M0, cl. gr. 2. Planned laboratory and instrumental studies were performed. Contraindications for surgical treatment were not identified. A preoperative course of chemotherapy was performed, against the background of which the patient's condition worsened with symptoms of acute cardiopathy. A second ECG was urgently performed, as a result of which an increase in the ST segment in III, aVF was established, as well as a study of the concentration of cardiomarkers: highly sensitive troponin I, N-terminal propeptide of natriuretic hormone, creatine phosphokinase MB, myoglobin, the dynamics of changes in the level of which indicated the development of acute coronary syndrome. The complex application of diagnostic procedures, including the determination of the level of cardiomarkers, made it possible to timely diagnose the development of acute type 1 myocardial infarction in a patient with tongue cancer on the background of chemotherapy. When analyzing the entire array of clinical and laboratory data, the leading initiating factor that played a decisive role in the development of myocardial infarction in this case was, in our opinion, a preoperative course of polychemotherapy with paclitaxel and carboplatin, which have cardiotoxicity. Thus, the category of patients with an initial unfavorable background, due to a common malignant process and the presence of a history of cardiodisfunction, requires more careful preparation for preoperative courses of polychemotherapy, including cardiotropic therapy with mandatory monitoring of the level of the main cardiomarkers. The most significant changes were in the levels of creatine phosphokinase MB, troponin I, and myoglobin, which were recorded in the first hours of myocardial infarction. An association was found between an increase in troponin I concentration and an increase in the ST segment of the electrocardiogram.

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Fursevich, Dzmitry, Colin Zuchowski, Joseph Limback, Melissa Kendall, Ashley Ramirez, Naim Fanaian, and Jeremy Burt. "Leukemic Ischemia: A Case of Myocardial Infarction Secondary to Leukemic Cardiac Involvement." Case Reports in Cardiology 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/7298347.

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We report a case of a 39-year-old male who presented to the emergency department with acute chest pain while being in remission from T-cell acute lymphoblastic leukemia (T-ALL). Cardiac markers were elevated and EKG revealed ischemic changes compatible with acute myocardial ischemia. Coronary computed tomography angiography (CCTA) showed calcium-free coronary arteries and soft tissue myocardial infiltration suggestive of cardiac leukemia. A bone marrow biopsy confirmed recurrence of T-ALL, and patient was successfully treated with chemotherapy. We discuss the prospective diagnosis of myopericardial leukemic involvement and the role of CCTA in diagnosis and perform a literature review.

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Cardinale, Daniela Maria, Martina Zaninotto, Carlo Maria Cipolla, Claudio Passino, Mario Plebani, and Aldo Clerico. "Cardiotoxic effects and myocardial injury: the search for a more precise definition of drug cardiotoxicity." Clinical Chemistry and Laboratory Medicine (CCLM) 59, no. 1 (January 26, 2021): 51–57. http://dx.doi.org/10.1515/cclm-2020-0566.

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AbstractDrug-induced cardiotoxicity is a major clinical problem; cardiotoxic drugs may induce both cardiac dysfunction and myocardial injury. Several recent studies reported that cardiac troponins measured with high-sensitivity methods (hs-cTn) can enable the early detection of myocardial injury related to chemotherapy or abuse of drugs that are potentially cardiotoxic. Several authors have some concerns about the standard definition of cardiotoxicity, in particular, regarding the early evaluation of chemotherapy cardiotoxicity in cancer patients. Several recent studies using the hs-cTn assay indicate that myocardial injury may precede by some months or years the diagnosis of heart failure (HF) based on the evaluation of left ventricular ejection fraction (LVEF). Accordingly, hs-cTn assay should considered to be a reliable laboratory test for the early detection of asymptomatic or subclinical cardiotoxic damage in patients undergoing cancer chemotherapy. In accordance with the Fourth Universal Definition of Myocardial Infarction and also taking into account the recent experimental and clinical evidences, the definition of drug-cardiotoxicity should be updated considering the early evaluation of myocardial injury by means of hs-cTn assay. It is conceivable that the combined use of hs-cTn assay and cardiac imaging techniques for the evaluation of cardiotoxicity will significantly increase both diagnostic sensitivity and specificity, and also better prevent chemotherapy-related left ventricular (LV) dysfunction and other adverse cardiac events. However, large randomized clinical trials are needed to evaluate the cost/benefit ratio of standardized protocols for the early detection of cardiotoxicity using hs-cTn assay in patients receiving chemotherapy for malignant diseases.

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TANOUE, Toshihide, Toshiro KAGESHITA, Satoshi FUKUSHIMA, Keishi MARUO, Shoji WAKASUGI, Tomomichi ONO, Hironobu IHN, and Hisao OGAWA. "Two cases with cutaneous melanoma who experienced acute myocardial infarction related to chemotherapy." Skin Cancer 21, no. 1 (2006): 36–40. http://dx.doi.org/10.5227/skincancer.21.36.

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Stoter, G., A. Koopman, C. P. Vendrik, A. Struyvenberg, D. T. Sleyfer, P. H. Willemse, H. Schraffordt Koops, A. T. van Oosterom, W. W. ten Bokkel Huinink, and H. M. Pinedo. "Ten-year survival and late sequelae in testicular cancer patients treated with cisplatin, vinblastine, and bleomycin." Journal of Clinical Oncology 7, no. 8 (August 1989): 1099–104. http://dx.doi.org/10.1200/jco.1989.7.8.1099.

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This 10-year follow-up study of 91 patients with disseminated testicular nonseminomatous cancer, treated with cisplatin, vinblastine, and bleomycin (PVB) induction chemotherapy and vinblastine plus bleomycin maintenance chemotherapy for a planned period of 2 years, shows a 63% cure rate. The predominant long-term sequelae are neurological and sexual dysfunction in 68% and 40% of patients, respectively. Two patients died of myocardial infarction. Sixteen percent of patients developed hypertension, 23% Raynaud's phenomenon, and 25% ototoxicity. Despite the long-term side effects, 90% of the patients who responded to a questionnaire are fully employed. This study shows that the maintenance chemotherapy has contributed to the incidence and/or degree of neurotoxicity, hypertension, and renal function disturbance.

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Mermershtain, W., J. Dudnik, I. Gusakova, and S. Ariad. "Acute Myocardial Infarction in a Young Man Receiving Chemotherapy for Testicular Cancer: Case Report." Journal of Chemotherapy 13, no. 6 (January 2001): 658–60. http://dx.doi.org/10.1179/joc.2001.13.6.658.

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Erol, Mustafa Kemal, Mahmut Acikel, and Huseyin Senocak. "Non-Q-Wave Acute Anterior Myocardial Infarction Associated with 5-Fluorouracil and Cisplatin Chemotherapy." Southern Medical Journal 96, no. 1 (January 2003): 99. http://dx.doi.org/10.1097/01.smj.0000047920.00535.2d.

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Kälsch, H., H. Wieneke, and R. Erbel. "Acute myocardial infarction in a patient with chronic myelocytic leukemia during chemotherapy with hydroxyurea." Herz 35, no. 6 (August 20, 2010): 420–22. http://dx.doi.org/10.1007/s00059-010-3367-6.

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Kobayashi, Hiroharu, Yoshifumi Arai, Kentaro Iga, Misa Kobayashi, Takashi Suzuki, Satoru Nakayama, and Hiroshi Adachi. "A Case of Trousseau’s Syndrome Accompanying Ovarian Cancer with Widespread Thromboembolisms." Case Reports in Obstetrics and Gynecology 2020 (June 5, 2020): 1–4. http://dx.doi.org/10.1155/2020/3738618.

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The patient was a 41-year-old woman, gravida 0. She had no notable medical history. Laparoscopic right salpingo-oophorectomy and left cystectomy were performed for bilateral ovarian endometriomas, which were both pathologically diagnosed as benign. Six months later, she presented with left lower abdominal pain and expressive aphasia. Examination revealed multiple cerebral infarctions and pulmonary embolism. The patient was diagnosed with Trousseau’s syndrome secondary to ovarian cancer, and anticoagulant therapy was initiated. Despite treatment, she developed visual field loss due to occlusion of the left retinal artery; dizziness due to cerebellar infarction and myocardial infarction; and right hemiplegia due to new cerebral infarction. She received chemotherapy (two courses of paclitaxel and carboplatin), which did not improve her condition, and died two months after onset. An autopsy revealed that her left ovary was enlarged to a size of 12 cm and an endometrioid carcinoma G2 was identified. Ovarian cancer had spread throughout the abdominal cavity, and a large amount of pleural and ascites fluid was present. Multiple thrombi were found in bilateral pulmonary arteries and bilateral common iliac veins. There was a 2.5 cm thrombus in the left ventricle apex, and the anterior descending branch was obstructed by thrombus with recanalization.

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Vogelzang, Nicholas J. "Antiangiogenic Agents, Chemotherapy, and the Treatment of Metastatic Transitional Cell Carcinoma." Journal of Clinical Oncology 31, no. 6 (February 20, 2013): 670–75. http://dx.doi.org/10.1200/jco.2012.44.4349.

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A 69-year-old man with a 100 pack-year history of smoking developed gross hematuria. His medical history included hypertension, a silent myocardial infarction, and a cerebrovascular accident complicated by seizures. Cystoscopy and biopsy showed a 4-cm mass at the right ureteral orifice positive for a high-grade papillary transitional cell carcinoma (TCC) with muscularis propria invasion (Fig 1). The computed tomography (CT)/positron emission tomography (PET) scan of the chest, abdomen, and pelvis showed hydronephrosis and hydroureter with marked cortical thinning and multiple bilateral PET-avid pulmonary nodules, with the largest in the left upper lung measuring 3.0 × 2.5 cm (Figs 2A, 3A), biopsy of which showed invasive high-grade urothelial carcinoma. The patient consented to join a clinical trial for metastatic TCC (USON [US Oncology Network study] 06040) involving treatment with gemcitabine, cisplatin, and sunitinib (GCS) 37.5 mg per day.1Four days later, he experienced a 10-day hospitalization for acute pancreatitis and neutropenia. Sunitinib was discontinued, and he completed four additional cycles of GC. CT/PET showed that the right ureteral mass and all lung nodules had regressed or disappeared (Figs 2B, 3B). The largest remaining lung nodule at 1.4 cm showed no metabolic activity. He underwent a radical cystoprostatectomy and right nephroureterectomy, disclosing residual high-grade urothelial carcinoma infiltrating the full thickness of the ureteral wall. There was carcinoma in situ of the bladder, and 42 nodes were negative for cancer. The surgery was followed by a small, uncomplicated myocardial infarction. A scheduled left thoracotomy to remove the remaining nodule was cancelled. No additional chemotherapy was administered, and the patient remains free of recurrence 2 years from initiation of chemotherapy. The 1.4-cm nodule has calcified and remains stable and metabolically inactive. He has no sequelae of chemotherapy or surgery, with a creatinine level of 1.35 mg/dL.

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Kawano, Naoko, Koji Yamaguchi, Toshiyuki Niki, Takashi Yamamoto, Takashi Iwase, Yoshio Taketani, Takayuki Ise, et al. "Two cases of acute myocardial infarction during combined chemotherapy in young patients with testicular cancer." Journal of Cardiology Cases 7, no. 6 (June 2013): e176-e180. http://dx.doi.org/10.1016/j.jccase.2013.02.009.

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Nichols, C. R., B. J. Roth, S. D. Williams, I. Gill, F. M. Muggia, D. M. Stablein, R. B. Weiss, and L. H. Einhorn. "No evidence of acute cardiovascular complications of chemotherapy for testicular cancer: an analysis of the Testicular Cancer Intergroup Study." Journal of Clinical Oncology 10, no. 5 (May 1992): 760–65. http://dx.doi.org/10.1200/jco.1992.10.5.760.

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PURPOSE The purpose of this study is to evaluate the risk of acute vascular events in patients receiving cisplatin-based chemotherapy for testicular cancer. PATIENTS AND METHODS A questionnaire assessing cardiovascular toxicity was distributed to all participants in the Testicular Cancer Intergroup study and details of toxicity from the chemotherapy flow sheets were reviewed. Patients with pathologic stage I testicular cancer were registered on to the study and observed after retroperitoneal lymphadenectomy. Patients with pathologic stage II disease were randomized to receive two postoperative courses of adjuvant cisplatin-based chemotherapy or observation. Any patient who had disease recurrence after observation or adjuvant therapy was given four cycles of cisplatin-based chemotherapy. RESULTS Review treatment-related toxicity for those patients receiving adjuvant chemotherapy (n = 97) or chemotherapy for recurrent disease (n = 83) showed no cases of acute cardiovascular toxicity. The median follow-up period after study enrollment was 5.1 years; 459 questionnaires were mailed and 270 were returned. The percent return was equal among the observed adjuvant and recurrent groups (59%, 54%, and 64%). There was a significant increase in the incidence of extremity paresthesias in the two groups receiving chemotherapy. Fatal myocardial infarction was reported in two patients in the observation group and one nonfatal infarction was reported in the adjuvant treatment group. No patient in any group reported an incidence of stroke. Three patients in the observation group and one patient in the recurrent group experienced a thromboembolic event. CONCLUSION Despite sporadic case reports suggesting a causal association between chemotherapy for testicular cancer and acute vascular events, this retrospective analysis provides no evidence of an increased risk for subsequent cardiovascular disease in this patient population.

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Scholz, K. H., C. Herrmann, U. Tebbe, J. M. Chemnitius, U. Helmchen, and H. Kreuzer. "Myocardial infarction in young patients with Hodgkin's disease ? potential pothogenic role of radiotherapy, chemotherapy, and splenectomy." Clinical Investigator 71, no. 1 (January 1993): 57–64. http://dx.doi.org/10.1007/bf00210966.

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Colovic, Natasa, Andrija Bogdanovic, Marijana Virijevic, Ana Vidovic, and Dragica Tomin. "Acute myocardial infarction during induction chemotherapy for acute MLL t(4;11) leukemia with lineage switch and extreme leukocytosis." Srpski arhiv za celokupno lekarstvo 143, no. 11-12 (2015): 734–38. http://dx.doi.org/10.2298/sarh1512734c.

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Introduction. In patients with acute leukemias hemorrhage is the most frequent problem. Vein thrombotic events may appear rarely but arterial thromboses are exceptionally rare. We present a patient with acute leukemia and bilateral deep leg vein thrombosis who developed an acute myocardial infarction (AMI) during induction chemotherapy. The etiology and treatment of AMI in patients with acute leukemia, which is a rare occurrence, is discussed. Case Outline. In April of 2012 a 37-year-old male presented with bilateral deep leg vein thrombosis and malaise. Laboratory data were as follows: Hb 118 g/L, WBC 354x109/L (with 91% blasts in differential leukocyte count), platelets 60?109/L. Bone marrow aspirate and immunophenotype revealed the presence of acute lymphoblastic leukemia. Cytogenetic analysis was as follows: 46,XY,t(4;11)(q21:q23) [2]/62-82,XY,t(4;11)[18]. Molecular analysis showed MLL-AF4 rearrangement. The patient was on low molecular weight heparin and combined chemotherapy according to protocol HyperCVAD. On day 10 after chemotherapy he got chest pain. Three days later AMI was diagnosed (creatine kinase 66 U/L, CK-MB 13U/L, troponin 1.19 ?g/L). Electrocardiogram showed the ST elevation in leads D1, D2, aVL, V5 and V6 and ?micro q? in D1. On echocardiography, hypokinesia of the left ventricle and ejection fraction of 39% was found. After recovering from AMI and restoring left ventricle ejection fraction to 59%, second course of HyperCVAD was given. The control bone marrow aspirate showed 88% of blasts but with monoblastic appearance. Flow cytometry confirmed a lineage switch from lymphoblasts to monoblasts. In further course of the disease he was treated with a variety of chemotherapeutic combinations without achieving remission. Eventually, palliative chemotherapy was administered to reduce the bulk of blasts. He died five months after the initial diagnosis. Conclusion. AMI in young adults with acute leukemia is a very rare complication which may occur in patients with very high white blood cell count in addition with presence of a CD56 adhesion molecule and other concomitant thrombophilic factors. The treatment of AMI in patients with acute leukemias should include antiplatelet and anticoagulant therapy, even with more aggressive methods depending on patient?s age and clinical risk assessment.

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Jao, Geoffrey T., Mary Ann Knovich, Rodney W. Savage, and David C. Sane. "ST-Elevation Myocardial Infarction and Myelodysplastic Syndrome with Acute Myeloid Leukemia Transformation." Texas Heart Institute Journal 41, no. 2 (April 1, 2014): 234–37. http://dx.doi.org/10.14503/thij-12-2905.

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Acute myocardial infarction and acute myeloid leukemia are rarely reported as concomitant conditions. The management of ST-elevation myocardial infarction (STEMI) in patients who have acute myeloid leukemia is challenging: the leukemia-related thrombocytopenia, platelet dysfunction, and systemic coagulopathy increase the risk of bleeding, and the administration of thrombolytic agents can be fatal. We report the case of a 76-year-old man who presented emergently with STEMI, myelodysplastic syndrome, and newly recognized acute myeloid leukemia transformation. Standard antiplatelet and anticoagulation therapy were contraindicated by the patient's thrombocytopenia and by his reported ecchymosis and gingival bleeding upon admission. He declined cardiac catheterization, was provided palliative care, and died 2 hours after hospital admission. We searched the English-language medical literature, found 8 relevant reports, and determined that the prognosis for patients with concomitant STEMI and acute myeloid leukemia is clearly worse than that for either individual condition. No guidelines exist to direct the management of STEMI and concomitant acute myeloid leukemia. In 2 reports, dual antiplatelet therapy, anticoagulation, and drug-eluting stent implantation were used without an increased risk of bleeding in the short term, even in the presence of thrombocytopenia. However, we think that a more conservative approach—balloon angioplasty with the provisional use of bare-metal stents—might be safer. Simultaneous chemotherapy for the acute myeloid leukemia is crucial. Older age seems to be a major risk factor: patients too frail for emergent treatment can die within hours or days.

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Huang, Wen Kuan, and Lai-Chu See. "Type of 5-fluorouracil and risk of cardiovascular events in early-stage colon cancer." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e15596-e15596. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e15596.

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e15596 Background: Older patients with colorectal cancer are at increased risk of developing cardiovascular (CV) disease. 5-FU-based chemotherapy was found to increase CV morbidity; however, whether CV risks differ among different fluorouracil types, including infusional 5-FU, capecitabine, and tegafur-uracil (UFT), remains unclear. We aimed to assess the association between CV morbidities, including myocardial infarction and heart failure, and different 5-FU types in patients with colorectal cancer. Methods: We evaluated patients from Taiwan Cancer Registry linked with national health insurance research database with stage I to III colorectal cancer between January 1, 2004, and December 31, 2014. A multivariate Cox proportional model with age as the time scale was conducted for comparison. UFT alone was set as the control group. Results: In the cohort of 29176 patients (median [interquartile range] age, 65 [43-79] years), 2241 (7.6%) received UFT, 25181 (86.3%) received infusional 5-FU or capecitabine, 1754 (6%) received mixed. Overall, 290 patients were diagnosed with myocardial infarction (1.78 per 1000 person-years) during a median (interquartile range) follow-up of 5.5 years. Compared with those received UFT, those using infusional 5-FU or capecitabine showed no increased risk of myocardial infarction (weighted hazard ratio [HR], 0.84; 95% CI, 0.57-1.24). There were 376 patients diagnosed with heart failure, corresponding to 2.3 per 1000 person-years. The risks of heart failure between the UFT group and infusional 5-FU/capecitabine were similar (weighted HR, 0.9; 95% CI, 0.62-1.31). Conclusions: In this study, we did not observe any increased CV risk using infusional 5-FU or capecitabine compared with UFT alone use.

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Sinitsky, M. Yu, A. V. Tsepokina, M. V. Khutornaya, A. V. Ponasenko, and A. N. Sumin. "Genetic basis of anthracyclines cardiotoxicity: Literature review." Acta Biomedica Scientifica 6, no. 4 (October 17, 2021): 27–38. http://dx.doi.org/10.29413/abs.2021-6.4.3.

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The purpose of this review was to systematize data on molecular genetic markers of increased risk of cardiotoxic effects, as well as to search for risk and protective variants of candidate genes. Today, the therapy of malignant neoplasms is based on the use of anthracyclines – drugs of the cytostatic mechanism of action. Along with their effectiveness, these drugs can have a cardiotoxic effect on cardiomyocytes by increasing the amount of reactive oxygen species and disrupting mitochondrial biogenesis. Pathological disorders lead to an increased risk of myocardial dysfunction and a number of other cardiovascular pathologies in patients receiving chemotherapy using anthracyclines. The cardiotoxic effect of anthracyclines leads to cardiomyopathy, heart failure, myocardial infarction, and thrombosis. Early detection of cardiotoxic damage leads to reducing the negative effects of these drugs due to changes in chemotherapy tactics. It is known that the risk of cardiotoxic myocardial damage is genetically determined and controlled by more than 80 genes. In this review, the description of basic molecules such as ATP-binding cassette transporters and solute carrier family (SLC transporters), carbonyl reductase, molecules of antioxidant defense, xenobiotic and iron metabolism was performed. In addition, a special attention is paid to the study of epigenetic and post-translational regulation. The available data are characterized by some inconsistency that may be explained by the ethnic differences of the studied populations. Thus, a more detailed research of various ethnic groups, gene-gene interactions between potential candidate genes and epigenetic regulation is necessary. Thus, understanding the contribution of genetic polymorphism to the development of cardiotoxicity will help to assess the individual risks of cardiovascular pathology in patients with various types of cancer, as well as reduce the risk of myocardial damage by developing individual preventive measures and correcting chemotherapy.

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Amichetti, Maurizio, Sebastiana Boi, Gianni Fellin, Sergio Maluta, Paolo Dalla Palma, and Lucio Luciani. "Small Cell Carcinoma of the Urinary Bladder. Report of two Cases and Review of the Literature." Tumori Journal 78, no. 6 (December 1992): 409–13. http://dx.doi.org/10.1177/030089169207800615.

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Undifferentiated small cell carcinoma of the bladder is a rare but aggressive subset of urinary tract neoplasms. Analogous to small-cell carcinoma of the lung, this tumor frequently exhibits neuroendocrine differentiation. We report the 92nd and 93rd case of small cell carcinoma of the bladder reported in the literature with characteristic cytologic, histologic, histochemical, and ultrastructural features. The patients were treated initially with chemotherapy, but after a brief clinical course died for progression of disease and for myocardial infarction, respectively. The pathologic and clinical features and therapeutic options of the cases described in the literature are reviewed.

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Sara, Jaskanwal D., Jasvinder Kaur, Ryan Khodadadi, Muneeb Rehman, Ronstan Lobo, Sakti Chakrabarti, Joerg Herrmann, Amir Lerman, and Axel Grothey. "5-fluorouracil and cardiotoxicity: a review." Therapeutic Advances in Medical Oncology 10 (January 1, 2018): 175883591878014. http://dx.doi.org/10.1177/1758835918780140.

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Fluoropyrimidines such as 5-fluorouracil (5-FU) form the foundation of a wide variety of chemotherapy regimens. 5-FU is in fact the third most commonly used chemotherapeutic agent in the treatment of solid malignancies across the world. As with all chemotherapy, balancing the potential benefits of therapy against the risks of drug-related toxicity is crucial when clinicians and patients make shared decisions about treatment. 5-FU is the second most common chemotherapeutic drug associated with cardiotoxicity after anthracyclines, which can manifest as chest pain, acute coronary syndrome/myocardial infarction or death. Nevertheless a widespread appreciation of 5-FU-related cardiotoxicity and its implications is lacking amongst clinicians. In this review, we outline the incidence, possible risk factors, and likely pathophysiological mechanisms that may account for 5-FU-related cardiotoxicity and also highlight potential management strategies for this poorly understood clinical entity.

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Tosun, Veysel, Necmettin Korucuk, Murat Bayrak, Mustafa Serkan Karakaş, and Refik Emre Altekin. "Acute inferior st segment elevation myocardial infarction due to chemotherapy in a young man with testicular cancer." Cumhuriyet Medical Journal 38, no. 4 (November 25, 2016): 345. http://dx.doi.org/10.7197/cmj.v38i3.5000155141.

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Kim, Kyung Ho, Woo Jung Park, Taek Man Nam, Duck Hyoung Yoon, Pil Seog Heo, Young Choel Doo, Kyu Rook Han, et al. "A Case of Acute Myocardial Infarction In Man Treated with Chemotherapy containing Doxorubicin for Non-Hodgkin Lymphoma." Korean Circulation Journal 31, no. 5 (2001): 507. http://dx.doi.org/10.4070/kcj.2001.31.5.507.

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Chaulin, Aleksey M., Yulia V. Grigorieva, Ivan N. Milutin, and Dmitry V. Duplyakov. "Non-coronarogenic causes of increased cardiac troponins in the practice of physicians (literature review)." Aspirantskiy Vestnik Povolzhiya 20, no. 1-2 (December 10, 2020): 49–61. http://dx.doi.org/10.17816/2072-2354.2020.20.1.49-61.

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Cardiac isoforms of troponins are the most sensitive and specific biomarkers of myocardial damage and new high-sensitivity methods can reveal very minor damages on the heart muscle. However, elevated troponin levels indicate cardiac damage, but do not define the cause of the damage. Therefore, cardiac troponin elevations are common in many disease states and do not necessarily indicate the presence of acute myocardial infarction. In clinical practice, interpretation of positive troponins may be challenging. In our article, we consider the main non-coronarogenic causes of increased cardiac troponins. The first part of the review discusses the mechanisms of increase and the diagnostic value of cardiac troponins during physical exertion, inflammatory and toxic myocardial injuries (endocarditis, myocarditis, sepsis), and renal failure. The second part of the literature review describes the mechanisms of increase and the diagnostic value of troponins in pulmonary thromboembolism, dissecting aortic aneurysms, neurogenic pathologies (stroke, subarachnoid hemorrhages), and treatment with cardiotoxic drugs (chemotherapy). Special attention is paid to the false positive causes of elevation of troponins.

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Boldig, Kimberly, Anupriya Ganguly, Meet Kadakia, and Abhinav Rohatgi. "Managing life-threatening 5-fluorouracil cardiotoxicity." BMJ Case Reports 15, no. 10 (October 2022): e251016. http://dx.doi.org/10.1136/bcr-2022-251016.

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5-Fluorouracil (5-FU), a known cardiotoxin, is the backbone for the treatment of colorectal cancer. It is associated with arrhythmias, myocardial infarction and sudden cardiac death. Most commonly, it is associated with coronary vasospasm secondary to direct toxic effects on vascular endothelium.A woman with metastatic colon cancer, originally treated with a 5-FU infusion as part of the FOLFIRI (Folinic acid, 5-Fluorouracil, Irinotecan) regimen, was unable to tolerate the chemotherapy due to chest pain. She was transitioned from infusional 5-FU to inferior 1-hour bolus 5-FU, in an attempt to minimise cardiotoxicity, but had disease progression. A multidisciplinary decision was made to again trial 5-FU infusion and pretreat with diltiazem. She tolerated chemotherapy without adverse events. A multidisciplinary discussion is recommended for co-management of reversible 5-FU-associated cardiotoxicity. After coronary artery disease (CAD) risk stratification and treatment, empiric treatment with calcium channel blockers and/or nitrates may allow patients with suspected coronary vasospasm, from 5-FU, to continue this vital chemotherapy.

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Basha, Sara Al, Najla Salkho, Sarah Dalibalta, and Ghaleb Adnan Husseini. "Liposomes in Active, Passive and Acoustically-Triggered Drug Delivery." Mini-Reviews in Medicinal Chemistry 19, no. 12 (July 12, 2019): 961–69. http://dx.doi.org/10.2174/1389557519666190408155251.

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Cancer has become one of the most deadly noncommunicable diseases globally. Several modalities used to treat cancer patients exist today yet many have failed to prove high efficacy with low side effects. The most common example of such modalities is the use of chemotherapeutic drugs to treat cancerous cells and deter their uncontrolled proliferation. In addition to the destruction of cancerous tissues, chemotherapy destroys healthy tissues as it lacks the specificity to annihilate cancerous cells only and preferentially, which result in adverse side effects including nausea, hair fall and myocardial infarction. To prevent the side effects of non-selective chemotherapy, cancer therapy research has been focused on the implementation of nanocarrier systems that act as vehicles to encapsulate drugs and selectively transport their agent to the tumor site. In this paper, we shed light on liposomes along with three anticancer drug delivery approaches: passive, active and ultrasound-triggered drug delivery.

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Chaulin, A. M., and D. V. Duplyakov. "High-sensitivity cardiac troponins: circadian rhythms." Cardiovascular Therapy and Prevention 20, no. 1 (February 19, 2021): 2639. http://dx.doi.org/10.15829/1728-8800-2021-2639.

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High-sensitivity cardiac troponins (hs-cTnI and hs-cTnT) contribute to a progression in the diagnosis and treatment of cardiovascular diseases: acceleration of diagnosis of acute myocardial infarction (early diagnostic algorithms: 0-1 h, 0-3 h), and earlier initiation of optimal treatment, expansion of diagnostic and prognostic potential (earlier detection of myocardial damage during chemotherapy, endocarditis, myocarditis and other diseases). However, increased sensitivity slightly reduced the specificity and created the need for a more thorough interpretation of elevated levels of hs-cTnI and hs-cTnT in a number of pathologies that damage cardiomyocytes. In addition, there was a need to introduce reference levels of hs-cTnI and hs-cTnT (99 percentile), taking into account sex. Recently, there has also been information about circadian (diurnal) variations in hs-cTnT and hs-cTnI levels. We analyze in detail the results of clinical studies that found circadian changes in hs-cTnI and hs-cTnT. Possible mechanisms underlying these changes in hs-cTnT and hs-cTnI concentrations are discussed.

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Lee, Kyoo Hyung, Jung Shin Lee, and Sang Hee Kim. "Electrocardiographic Changes Simulating Acute Myocardial Infarction or Ischemia Associated with Combination Chemotherapy with Etoposide, Cisplatin, and 5-Fluorouracil." Korean Journal of Internal Medicine 5, no. 2 (July 31, 1990): 112–18. http://dx.doi.org/10.3904/kjim.1990.5.2.112.

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Nagatomo, D., J. i. Oyama, M. Yoshihara, and K. Node. "Successful treatment of primary cardiac lymphoma causing ST-elevation myocardial infarction by percutaneous coronary intervention combined with chemotherapy." Case Reports 2014, no. 17 1 (November 17, 2014): bcr2014207267. http://dx.doi.org/10.1136/bcr-2014-207267.

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Morrow, Andrew J., Alan C. Cameron, Alexander R. Payne, Jeff White, and Ninian N. Lang. "Cisplatin related cardiotoxicity – acute and chronic cardiovascular morbidity in a testicular cancer survivor." Scottish Medical Journal 65, no. 1 (December 30, 2019): 24–27. http://dx.doi.org/10.1177/0036933019897347.

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Testicular germ cell tumours are the most common malignancy in men aged 20 to 40 years. They are subdivided into seminoma and non-seminomatous germ cell tumours (NSGCTs). Both seminoma and NSGCT occur at about the same rate, however some tumours contain a combination of both. Cisplatin-based chemotherapy is used adjuvantly in high-risk stage 1 mixed and NSGCT patients and contributes towards oncological cure in almost all metastatic cases, regardless of histology. However, cardiovascular toxicity is a major concern. In addition to acute endothelial toxicity and associated risk of arterial thrombosis, accelerated atherosclerosis may be the result of chemotherapy-associated latent cardio-metabolic dysfunction. A 45-year-old man began treatment with cisplatin-based chemotherapy for testicular cancer. On day 9, he suffered an anterior ST segment elevation myocardial infarction (STEMI). There was proximal occlusion of the left anterior descending (LAD) artery but otherwise normal coronary arteries. Ten months following chemotherapy, he had another STEMI. There was a fresh obstructive lesion in the previously angiographically normal mid LAD, new diffuse coronary atheroma elsewhere and a deterioration in lipid profile despite statin therapy. Acute and longer-term cardiovascular risks of cisplatin-based chemotherapy may have different underlying pathophysiological mechanisms. These issues are of growing relevance in a population of patients expected to have excellent cancer-related outcomes.

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Jurczyk, Michał, Magdalena Król, Aleksandra Midro, Magdalena Kurnik-Łucka, Adrian Poniatowski, and Krzysztof Gil. "Cardiotoxicity of Fluoropyrimidines: Epidemiology, Mechanisms, Diagnosis, and Management." Journal of Clinical Medicine 10, no. 19 (September 27, 2021): 4426. http://dx.doi.org/10.3390/jcm10194426.

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Cancer is a growing public health problem; it is responsible annually for millions of deaths worldwide. Fluoropyrimidines are highly effective and commonly prescribed anti-neoplastic drugs used in a wide range of chemotherapy regimens against several types of malignancies. 5-fluorouracil and its prodrugs affect neoplastic cells in multiple ways by impairing their proliferation, principally through the inhibition of thymidylate synthase. Fluoropyrimidine-induced cardiotoxicity was described more than 50 years ago, but many details such as incidence, mechanisms, and treatment are unclear and remain disputed. Severe cardiotoxicity is not only life-threatening, but also leads to withdrawal from an optimal chemotherapy regimen and decreases survival rate. Differences in the frequency of cardiotoxicity are explained by different chemotherapy schedules, doses, criteria, and populations. Proposed pathophysiological mechanisms include coronary vasospasm, endothelial damage, oxidative stress, Krebs cycle disturbances, and toxic metabolites. Such varied pathophysiology of the cardiotoxicity phenomenon makes prevention and treatment more difficult. Cardiovascular disturbances, including chest pain, arrhythmias, and myocardial infarction, are among the most common side effects of this class of anti-neoplastic medication. This study aims to summarize the available data on fluoropyrimidine cardiotoxicity with respect to symptoms, incidence, metabolism, pathophysiological mechanism, diagnosis, management, and resistance.

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Meinardi, M. T., J. A. Gietema, W. T. A. van der Graaf, D. J. van Veldhuisen, M. A. Runne, W. J. Sluiter, E. G. E. de Vries, et al. "Cardiovascular Morbidity in Long-Term Survivors of Metastatic Testicular Cancer." Journal of Clinical Oncology 18, no. 8 (April 8, 2000): 1725–32. http://dx.doi.org/10.1200/jco.2000.18.8.1725.

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PURPOSE: To determine whether long-term survivors of metastatic testicular cancer have an increased risk of cardiovascular morbidity more than 10 years after chemotherapy.PATIENTS AND METHODS: Eighty-seven patients treated with cisplatin-containing chemotherapy before 1987 who were in remission for at least 10 years and whose ages were ≤ 50 years at the time of analysis were evaluated for the occurrence of cardiovascular events. Sixty-two of 87 patients were additionally evaluated for cardiac damage and cardiovascular risk factors. Their cardiovascular risk profile was compared with that of 40 patients with comparable age and follow-up duration treated with orchidectomy only for stage I disease.RESULTS: Major cardiac events were found in five (6%) of the 87 patients (age at time of event, 30 to 42 years; time after chemotherapy, 9 to 16 years): two with myocardial infarction and three with angina pectoris with proven myocardial ischemia. An increased observed-to-expected ratio of 7.1 (95% confidence interval, 1.9 to 18.3) for coronary artery disease, as compared with the general male Dutch population, was found. In addition, one patient experienced a cerebrovascular accident. Exercise ECG did not reveal cases of subclinical coronary artery disease. Echocardiography showed normal systolic left ventricular function in most patients, but diastolic left ventricular function was disturbed in 33% of the patients. Of 62 chemotherapy patients, 79% had hypercholesterolemia, 39% had hypertension, 25% still experienced Raynaud’s phenomenon, and 22% had microalbuminuria. Compared with patients with stage I disease, the chemotherapy patients had higher blood pressure and higher total cholesterol and triglyceride levels and were more insulin-resistant.CONCLUSION: In long-term survivors of metastatic testicular cancer, we observed a significantly increased risk for occurrence of cardiac events accompanied by a persisting unfavorable cardiovascular risk profile. Accurate follow-up, focused on cardiovascular complications and aimed at intervention in these young cancer survivors, seems to be important.

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Ivovic, Miomira, Biljana Radojkovic, Zorana Penezic, Mirjana Stojkovic, Milina Tancic, Svetlana Vujovic, Andrija Bogdanovic, and Milka Drezgic. "Agranulocytosis and acute coronary syndrom in apathetic hyperthyreoidism." Srpski arhiv za celokupno lekarstvo 131, no. 5-6 (2003): 249–53. http://dx.doi.org/10.2298/sarh0306249i.

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INTRODUCTION Tissue expose to excessive levels of circulating thyroid hormones results in thyrotoxicosis. In most cases, thyrotoxicosis is due to hyper-activity of the thyroid gland. Cardiovascular and myopathic manifestations are predominant clinical features in most hyperthyroid patients, aged 60 years and older. Some of patients have apathetic hyperthyreoidism which presents with weight loss, small goiter, severe depression and without clinical features of increased sympathetic activity [3, 6]. About 50% of patients with cardiovascular manifestations have no evidence of underlying heart disease. Cardiac problems resolve when euthyreoid state is established [3]. Three treatment modalities are available in hyperthyreodism, namely medicament therapy, surgery and radioactive iodine. Antithyroid drug therapy complications, can be mild such as rash, which is managed without cessation of therapy by antihistamines administration. On the other hand, very serious complications such as agranulocytosis, necessitate immediate discontinuation of the medication and appropriate treatment. Although extremely rear, it is life-threatening with highly variable recovery time. CASE REPORT A 62-year-old woman with recurrent hyperthyroidism was admitted after treatment of agranu locytosis due to antithyroid drugs in another institution with G-CSF. The patient presented with clinical features of apathetic hyperthyroidism with extremely elevated thyroid hormone levels (total and free T4) and suppressed TSH. Radioactive iodine (5 mCi) was administered after increased thyroid uptake was confirmed. Echocardiography on admission was normal. ECG revealed moderately inverted T waves in standard and V1, V2 precordial leads. Laboratory analysis revealed mild normocytic anemia with normal white blood cell count, hypokaliemia and normal concentration of creatine phosphokinase lactic dehidrogenase and mildly elevated aspartate transaminase in sera. Chest X-ray was consistent with pulmonary emphysema. Because the worsening of ECG changes she was transferred to Coronary unit. The diagnosis of non-Q myocardial infarction was confirmed and treatment with nitrates and beta-adrenergic antagonists was instituted. Four weeks later she became euthyroid and coronarography was performed. Subepicardial coronary arteries were normal (Figure 1). She was dismissed, and still euthyroid three months later. DISCUSSION Agranulocytosis is very rare but very serious complication of antithyroid drug therapy. It can be detected in about 0.1 -1 % patients during the first three months of treatment. Sudden appearance, heralded by sore throat and fever, prompt physicians to seek white blood cell and differential count [1-3]. Confirmation of diagnosis urges cessation of drug therapy and appropriate antibiotic treatment. Recently, it was reported that recombinant human granulocyte colony-stimulating factor (rhG-CSF) is to be effective in shortening the recovery time in the neutropenic patients undergoing chemotherapy and also in patients with other types of neutropenia [5]. Tamai at al. [7] confirmed positive outcome in 34 patients treated with rhG-CSF compared to corticosteroid treatment. Hematologic laboratory abnormalities disappear 7-10 days after secession of therapy. Patients completely recover two to three weeks later. Fatal outcome was also described [1 -5]. Thyroid hormones have profound effects on cardiovascular physiology, especially on heart rate, cardiac output and systemic vascular resistance. In patients with hyperthyroidism, cardiac output is much higher than in normal persons. This is the result of direct effect of thyroid hormones on cardiac muscle contractility, heart rate and decrease in systemic vascular resistance. Excessive thyroid hormone secretion increases cardiac Na-K-activated plasma membrane ATP-ase and sarcoplasmic reticulum Ca-activated ATP-ase with resultant in increase myocardial contractility [6 9]. Sinus tachycardia is the most common rhythm disorder in hyperthyroidism but paroxysmal tachycardia and atrial fibrillation are not rare. This can be explained by increased heart rate, cardiac output, blood volume, coronary artery flow and peripheral oxygen consumption in thyreotoxicosis [9]. Patients with coronary arteriosclerosis can develop angina pectoris during thyreotoxic stage, which can be explained by imbalance between cardiac demand and supply. Myocardial damage is often in thyrotoxic patients with chronic hart failure, together with myocardial infarction in patients without coronary disease [2,6]. Congestive heart failure and atrial fibrillation are relatively resistant to digitalis treatment because of high metabolic turn over of medication and excessive myocardial irritability in hyperthyro-idism [6]. Cardiovascular and myopathic manifestations predominate in older hyperthyroid patients (over 60 years) and some of them can have only few symptoms of hyperthyroidism [1-3]. Thyrotoxic state characterized by fatigue, apathy, extreme weakness, low-grade fever and sometimes congestive heart failure are designated as apathetic hyperthyroidism. Such patients have small goiters, mild tachycardia and often cool and dry skin with few eye signs [6]. Patients with subclinical hyperthyroidism are at increased risk for atrial fibrillation [9]. Unstable angina and non-Q myocardial infarction (non ST elevation) are acute manifestation of coronary artery disease. The acute coronary syndrome of unstable angina, non-Q myocardial infarction and Q-wave myocardial infarction have atherosclerotic lesions of the coronary arteries as a common pathogenic substrate. Errosions or ruptures of unstable atherosclerotic plaque triggered pathophysiologic processes, resulted in thrombus formation at the site of arterial injury. This leads to abrupt reduction or cessation through the affected vessel. Clinical manifestations of unstable angina and non-Q myocardial infarction are similar and diagnosis of non-Q myocardial infarction is made on the basis of elevated serum markers indicative of cardiac necrosis, detected in peripheral circulation. Acute coronary syndrome ranging from unstable angina to myocardial infarction an non-Q myocardial infarction represents increasingly severe manifestations of the same pathophysiologic processes [10,11]. In conclusion, these 62-year-old woman presented with apathetic form of recurrent hyperthyroidism associated with two serious complications life-threatening agranulocytosis and acute coronary syndrome.

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Jurczak, Wojciech, Marcin Sobocinski, Jagoda Gorka, Jacek Cieslak, Joanna Drozd-Sokolowska, Piotr Boguradzki, Justyna Dzietczenia, et al. "High Incidence of Cardiovascular Complications After CHOP-Like Chemotherapy In Lymphoma Patients From Poland – Retrospective Analysis of Polish Lymphoma Research Group (PLRG)." Blood 116, no. 21 (November 19, 2010): 1764. http://dx.doi.org/10.1182/blood.v116.21.1764.1764.

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Abstract Abstract 1764 Introduction: Cardiovascular System disorders are among the leading causes of mortality in general population ranging from 10% in Sub Saharan Africa, 38 % in Western Europe and US to even 58% in Eastern Europe and Central Asia. CHOP and it's modifications, with or without Rituximab is the most frequently used chemotherapy regimen for lymphoma patients. Antharcyclin related cardiotoxicity is a well described, dose dependent adverse effect, increasing in frequency with time after therapy, described in 3–5% of patients at 5 years to even 15% of patients at 10 or more years after diagnosis. It was postulated, that higher incidence of cardiovascular mortality, may increase the frequency of anthracyclin cardiotoxicity in Central Europe. Materials and Methods: A retrospective analysis was performed to investigate the frequency of cardiovascular complications after CHOP-like chemotherapy in 428 lymphoma patients treated in 5 oncohematological centers. The median observation time was 3 years (range 0.5–8), therefore it covered acute and early chronic progressive cardiotoxicity. Patients characteristics: average age 55 years (range 18–90), male to female ratio 221/207, clinical stage III/IV – 347 cases (81.5%), general symptoms – 302 cases (71%), large tumor burden defined as it's diameter of 10 cm or more – 41 cases (8.5%), IPI 3–5 in 174 cases (40%). There were 320 patients with DLBCL, 45 – MCL, 32 – FL, 24 – PTCL and 7 – MZL. Initial assessment was based on medical histories including echocardiography in 166 cases (38%). All patients were contacted at the time of analysis, and questioned in detail about symptoms and signs of left ventricular failure (LVF). Results: At a time of diagnosis risk factors for cardiovascular disorders were identified: arterial hypertension (29%), hypercholesterolaemia (13%), diabetes mellitus (8.2%), truncal obesity (17%) and smoking (18.5%). Minority of patients had a previous history of LVF (n=10, 2.3%) and/or myocardial infarction (n=6, 1.4%). The average dose of anthracyclins was 336,5 mg/m2 (range 50 – 680): 391 (91.9%) patients received Doxorubicin, 17 (3.9%) – Nonpegylated Liposomal Doxorubicin, 13 (3,1%) – Farmorubicin and 5 (1.1%) Dauborubicin. Acute cardiotoxicity was reported in 21 cases (4,9%) and resulted in dose reduction, postponing chemotherapy or it's premature termianation. The overall response rate was reasonable, with 297 (69.5%) CR, 83 (19.5%) PR, 10 (2.2%) SD and 38 (8.8%) progressions. At the time of analysis 100 patients (23.4%) relapsed and 63 (14.7%) died: 29 due to disease progression, 24 due to cardiovascular disease, 7 due to infectious complications and 3 due to unknown causes. The average Left Vetricular Ejection Fraction (LVEF), assessed by echochardiography in 166 patients decreased from 63% (range 42–85%) at diagnosis to 56,8% (range 20–72%) at the end of treatment (p<0.001). It corresponded to clinical picture: 51 patients (11.7%) required cardiological treatment after chemotherapy, including 15 cases (3.5%) with myocardial infarction, and further 37 (8.6%) with ischaemic heart pain. Even more revealed signs and symptoms of LVF on direct questioning: exertional dyspnea – 67 (15.7%), pretibial oedema – 72 (16.8%), Nycturia – 48 (11.2%). Conclusions: Our retrospective analysis revealed an important role of anthracyclin cardiotoxicity in lymphoma patients from Poland. At relatively short average time of observation (3 years, range 0.5–8), cardiovascular disorders were the second most common cause of death (24/63 – 38% of deaths, 24/428 – 5.6% of all cases). Further 51 patients (11.7%) required cardiological treatment for at least one life threatening event (myocardial infarction or ischaemic heart pain). Disclosures: No relevant conflicts of interest to declare.

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Voutsadakis, Ioannis, and Athina Stravodimou. "Statins use and peripheral blood progenitor cells mobilization in patients with multiple myeloma." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e17007-e17007. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e17007.

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e17007 Background: Statin drugs have beneficial effects in patients after myocardial infarction and at least part of the benefit is believed to result from mobilization of marrow endothelial progenitors to repopulate damage myocardial tissues. This study examines if statins may have the same effect in mobilizing marrow progenitors to be harvested and subsequently used in high dose chemotherapy with progenitor cell rescue in patients with multiple myeloma. Methods: From 2006 to 2009, 22 consecutive patients with multiple myeloma were mobilized with the use of G-CSF and were retrospectively analyzed. Patients with other malignancies or mobilized with the use of chemotherapy or with plerixafor were excluded from this analysis. Results: The median age of the patients was 60 years-old. Fifteen patients had received one line of chemotherapy, six patients two lines and one patient three lines of chemotherapy. Thirteen patients were taking statins at the time of the harvest while nine patients were not. In the group of patients taking statins in only two of 13 (15%) the target number of 4x106 CD34+ cells /kg could not be obtained with a single apheresis session while in the group not taking statins four of nine patients (44.5%) required more than one session to obtain this target (including one patient in whom the target number could not be obtained even with the additional sessions). Nevertheless due to the low number of patients in the study this difference did not attain statistical significance (x2=0.13). The median number of cells harvested was 8x106 CD34+ cells /kg in the group taking statins and 6.3x106 CD34+ cells /kg in the control group. Conclusions: This retrospective analysis of 22 patients discloses a numerically important difference in the success of peripheral blood progenitors harvest in patients taking statins which did not attain statistical significance. Larger studies would be required to clarify the issue. If their effectiveness is confirmed statins could be a safe and cheaper addition to chemotherapy and plerixafor for peripheral hematopoietic stem cell mobilization.

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Pan, Xianying, Devashish Verma, Jiayin Zhang, Yifan Zhang, and Xiaomei Ma. "Factors associated with the occurrence of myocardial infarction in patients treated for melanoma." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 10562. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.10562.

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10562 Background: Treatments for melanoma increasingly involve the use of immune checkpoint inhibitors (ICIs), which are associated with cardiac toxicities. Our study aims to examine predictors of myocardial infarction (MI) in melanoma patients receiving treatment. Methods: The United Healthcare (Optum Clinformatics) Closed Claims + Lab Results Database (01/2007 – 03/2021) was used to examine factors potentially associated with the occurrence of hospitalized MI in melanoma patients. Adult patients were included if they: 1) had ≥12 months of continuous insurance coverage at baseline; 2) had ≥2 outpatient or ≥1 inpatient claims with an International Classification of Diseases (ICD) code indicative of melanoma; 3) received ≥1 type of cancer treatment (surgery, chemotherapy, radiotherapy, ICI, or targeted therapy); 4) had a claim with a melanoma ICD code within 5 days before the first cancer treatment; and 5) had no history of MI at baseline. Baseline was defined as the year prior to the first date of treatment; MI occurrence was identified from inpatient claims. We conducted a time-to-event (MI) analysis using a multivariate Cox proportional hazards regression model, with backward selection and death as a competing risk. Results: A total of 42,101 patients (58.8% male; median age of 68 yrs at baseline) were included in the study. Of these, 954 patients (2.3%) experienced a MI, and 5,578 (13.2%) died before having a MI. Compared with patients who underwent surgery only, those who received multiple treatments with an ICI were more likely to have a MI (hazard ratio [HR] = 1.25, 95% confidence interval [CI]: 1.01-1.55; Table). Men had a higher risk than women (HR = 1.47, 95% CI: 1.27-1.71), as did older people (compared with 65-74-yr-olds, HRs were 0.24, 0.49, 1.41, and 2.06 for <55-, 55-64-, 75-84-, and ≥85-yr-olds, respectively; all P<.05). Being Asian and having certain comorbidities at baseline were also associated with a higher MI risk (Table). Conclusions: In this retrospective cohort analysis of patients with melanoma, we observed an increased risk of MI among patients who received multiple treatments with ICIs, compared with surgery only. More research is needed to further elucidate predictors of MI events related to cancer treatment. [Table: see text]

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Zerna, Charlotte, Michael Guenther, Gunnar Folprecht, and Volker Puetz. "Acute ischaemic stroke and myocardial infarction after chemotherapy with vinorelbine for non-small cell lung cancer: a case report." Journal of Chemotherapy 29, no. 1 (July 22, 2016): 49–53. http://dx.doi.org/10.1179/1973947814y.0000000232.

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Meyerhardt, Jeffrey A., Ling Li, Hanna K. Sanoff, William Carpenter, and Deborah Schrag. "Effectiveness of Bevacizumab With First-Line Combination Chemotherapy for Medicare Patients With Stage IV Colorectal Cancer." Journal of Clinical Oncology 30, no. 6 (February 20, 2012): 608–15. http://dx.doi.org/10.1200/jco.2011.38.9650.

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Purpose Clinical trials have shown that adding bevacizumab to cytotoxic chemotherapy improves survival for patients with colorectal cancer, although its effectiveness in the Medicare population is uncertain. Patients and Methods Using the Surveillance, Epidemiology, and End Results (SEER) -Medicare linked database, we identified 2,526 patients with stage IV colorectal cancer diagnosed between 2002 and 2007 who received first-line combination chemotherapy with a fluoropyrimidine and either irinotecan (33%) or oxaliplatin (67%). Thirty-six percent of patients received bevacizumab with first-line therapy. The primary outcome was overall survival. Secondary outcomes were bevacizumab-associated toxicities, including the incidence of stroke, myocardial infarction, and GI perforation. Results In the primary cohort inclusive of patients diagnosed between 2002 and 2007, bevacizumab with combination chemotherapy was associated with improved overall survival (adjusted hazard ratio [HR], 0.85; 95% CI, 0.78 to 0.93), although the effect was more modest when restricted to years 2004 to 2007 (HR, 0.93; 95% CI, 0.84 to 1.02). The observed survival advantage of bevacizumab was more apparent with irinotecan-based chemotherapy (HR, 0.80; 95% CI, 0.66 to 0.97) than with oxaliplatin-based chemotherapy (HR, 0.96; 95% CI, 0.86 to 1.07). Combination chemotherapy with bevacizumab, versus combination chemotherapy without bevacizumab, was associated with increased risk of stroke (4.9% v 2.5%, respectively; P < .01) and GI perforation (2.3% v 1.0%, respectively; P < .01). Cardiac events and venous thrombosis were not increased with bevacizumab. Conclusion The addition of bevacizumab to cytotoxic combination chemotherapy was associated with small improvement in overall survival as well as increased risk of stroke and perforation, but not cardiac events, among Medicare beneficiaries with stage IV colorectal cancer.

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Prasad, Megha, Michel T. Corban, Timothy D. Henry, Allan B. Dietz, Lilach O. Lerman, and Amir Lerman. "Promise of autologous CD34+ stem/progenitor cell therapy for treatment of cardiovascular disease." Cardiovascular Research 116, no. 8 (February 5, 2020): 1424–33. http://dx.doi.org/10.1093/cvr/cvaa027.

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Abstract CD34+ cells are haematopoietic stem cells used therapeutically in patients undergoing radiation or chemotherapy due to their regenerative potential and ability to restore the haematopoietic system. In animal models, CD34+ cells have been associated with therapeutic angiogenesis in response to ischaemia. Several trials have shown the potential safety and efficacy of CD34+ cell delivery in various cardiovascular diseases. Moreover, Phase III trials have now begun to explore the potential role of CD34+ cells in treatment of both myocardial and peripheral ischaemia. CD34+ cells have been shown to be safe and well-tolerated in the acute myocardial infarction (AMI), heart failure, and angina models. Several studies have suggested potential benefit of CD34+ cell therapy in patients with coronary microvascular disease as well. In this review, we will discuss the therapeutic potential of CD34+ cells, and describe the pertinent trials that have used autologous CD34+ cells in no-options refractory angina, AMI, and heart failure. Lastly, we will review the potential utility of autologous CD34+ cells in coronary endothelial and microvascular dysfunction.

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Chen, Gong, Jianjun Peng, Chao Dong, Meng Qiu, Chang Wang, Hua wei Li, Hao Yu, et al. "Cardiotoxicity in Chinese cancer patients treated with 5-fluorouracil or capecitabine: A multicenter prospective observational study." Journal of Clinical Oncology 35, no. 4_suppl (February 1, 2017): 553. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.553.

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553 Background: Although the cardiotoxicity associated with 5-Fluorouracil (5-FU) or capecitabine administration has been well addressed in literature, there is still a lack of data from prospective clinical trials in Chinese population. The aim of this study was to evaluate the incidence, manifestations and predisposing factors for the cardiotoxicity in Chinese cancer patients treated 5-FU or capecitabine. Methods: A multicenter prospective observational study was performed in 527 patients with various solid tumors from 12 cancer centers in china . Of these patients, 196 received 5-FU-based and 331 received oral capecitabine-based chemotherapy as either first-line or adjuvant therapy. Outcome measures including electrocardiogram(ECG), myocardial enzymes, cardiac troponin(cTn), BNP and echocardio- graphy(UCG) etc. Univariate analysis and the logistic regression were performed for subgroup analysis and identification of the significant independent variables that are associated with cardiotoxicity of both agents. Results: In total, 161 of 527 patients (30.55%) experienced cardiotoxicity. The incidence of cardiotoxicity was 33.84% (112 out of 331) in the capecitabine-treated population, significantly higher than 25 %( 49 out of 196) in the 5-FU treated population (P = 0.0042). 110 out of 527 patients (20.87%) suffered arrhythmia, 105/527 (19.92%) developed ischemic changes, while 20/527(3.80%) heart failure and 6/527 (1.14%) myocardial infarction only. Among the factors evaluated with univariate analysis and the logistic regression, a history of cardiac disease, chemotherapy agent, duration of treatment and hypertension were significant with cardiotoxicity occurrence. The odds ratio were 15.447(with a history of cardiac history vs without), 2.118 (Capecitabine group vs 5-FU group), 1.079(5-8 vs 1-4 cycles) and 1.698 (with hypertension vs without) respectively. Conclusions: Cardiotoxicity induced by fluoropyrimidines in Chinese population may be underestimated in clinical practice.Possible risk factors are duration of treatment, chemotherapy agents, preexisting cardiac disease and hypertension.

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Soyland, Dallas J., Dylan R. Goehner, Kayla M. Hoerschgen, Troy D. Gust, and Shawn M. Vuong. "Hemorrhagic spinal melanotic schwannoma presenting as acute chest pain: A case report and literature review." Surgical Neurology International 12 (April 14, 2021): 164. http://dx.doi.org/10.25259/sni_786_2020.

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Background: Melanotic schwannoma (MS) is a rare variant of peripheral nerve sheath tumor. MS commonly arises along the spinal nerve sheath. Patients most often experience pain along the dermatome of the affected nerve root. Symptoms development is usually insidious. About half of MS cases are associated with Carney complex, a multi-neoplastic disorder. The remaining cases arise spontaneously. About 10–44% of these tumors undergo malignant transformation. Case Description: We describe a case of hemorrhagic MS presenting as acute chest pain mimicking myocardial infarction, a presentation which has not yet been described in the literature. Neurologic examination did not reveal any abnormalities. Myocardial infarction was ruled out in the ER, and a chest CT angiogram was ordered for evaluation of PE or aortic dissection which revealed an intradural extramedullary dumbbell-shaped mass extending through the left vertebral foramen at the level of T8. MRI revealed a heterogenous mass that was hyperintense with T2 and hypointense with T1-weighted imaging. The patient underwent an open laminectomy of the left T8 and T9 vertebrae and gross total resection (GTR) of a hemorrhagic black tumor. Microscopic examination showed fascicles and nests of plump spindle cells with variable intracellular melanin. Immunohistochemistry showed the cells to be positive for S100, SOX10, HMB-45, and MART-1, confirming diagnosis of MS. Two months after the operation, the patient was doing well and is free of recurrence. Conclusion: GTR is considered the optimal treatment for MS; radiotherapy and chemotherapy may be considered but have not been shown to improve patient outcomes.

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Journal articles on the topic 'Myocardial infarction Chemotherapy'

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