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1
A, Raineri, Leachman Robert D, Kellermann Jan J, and International School of Cardiology (4th : 1986 : Ettore Majorana Centre for Scientific Culture), eds. The State and future directions of acute myocardial infarction: Proceedings of a course held at the International School of Medical Sciences, Ettore Majorana Centre for Scientific Culture, Italy, 2-7 April 1986. Chur, Switzerland: Harwood Academic Publishers, 1988.
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2
Müller-Schreiber, Sabine Christine. Myokardinfarkt und Leistungsmotivation. Frankfurt am Main: P. Lang, 1988.
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3
Inoue, Michitoshi. Kokuritsu byōin, ryōyōjo ni okeru konpyūta nettowāku o mochiita shinkin kōsoku no 1-ji, 2-ji yobō to kosuto benefitto ni kansuru tashisetsu maemuki kenkyū: Heisei 12-nendo sōkatsu kenkyū hōkokusho. [Japan: s.n.], 2001.
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4
Gross, Dawn H. Progressive muscular relaxation and rational-emotive therapy during the rehabilitation of survivors of first episode myocardial infarction classified as type A. Manchester: UMIST, 1997.
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5
The behavioral management of the cardiac patient. Norwood, N.J: Ablex Pub. Corp., 1987.
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6
A fatal chapter. Waterville, Maine: Thorndike Press, 2015.
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7
King, Stephen. El umbral de la noche. Barcelona, Spain: Plaza y Janés, 2001.
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8
King, Stephen. Night Shift. New York: Knopf Doubleday Publishing Group, 2008.
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9
King, Stephen. Night shift. New York: Anchor Books, 2012.
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10
Danse macabre. Paris: J'ai lu, 2002.
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11
King, Stephen. Night Shift. New York, USA: Anchor Books, 2011.
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12
King, Stephen. Night Shift. London: New English Library, 1986.
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13
King, Stephen. Night shift. Oxford: ISIS Large Print, 1994.
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14
King, Stephen. Night shift. Thorndike, Me: G.K. Hall, 1994.
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15
King, Stephen. Night Shift. New York, USA: New American Library, 1990.
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16
King, Stephen. Night Shift. New York, USA: New American Library, 1986.
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17
Sekhar, Rajagopal V. Dyslipidemia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0047.
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Patients infected with HIV often develop dyslipidemia. Although lipid abnormalities have been described in HIV-infected patients from the pre-combination antiretroviral therapy era, they are most striking in patients treated with antiretroviral drugs and may even be present in those not exposed to these drugs. The dyslipidemic profile in HIV includes abnormalities in lipids and lipoprotein, including hypertriglyceridemia, elevated plasma total low-density lipoprotein cholesterol concentrations, and low levels of high-density lipoprotein cholesterol. Many patients also have the phenotypic appearance of lipodystrophy, with a variable combination of centripetal fat accumulation. The consequence of an abnormal dyslipidemic profile in the HIV lipodystrophic patient is an accelerated risk of developing myocardial infarction, cardiovascular disease, nonalcoholic fatty liver disease, and type 2 diabetes.
18
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
19
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
20
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
21
Stevens, Victoria E. PERSONALITY TYPE AND WAYS OF COPING: A STUDY OF FEMALE SPOUSES OF POST-MYOCARDIAL INFARCTION PATIENTS (WIVES, MYOCARDIAL INFARCTION). 1992.
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22
Stone, Mike. Living with Restenosis 2-in-1-book : Includes : Surviving a Successful Heart Attack -and- the Next 20,000: After the Heart Attack, the Statins and Restenosis. Lulu Press, Inc., 2008.
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23
Barold, S. Serge. Atrioventricular conduction abnormalities and atrioventricular blocks: ECG patterns and diagnosis. Edited by Giuseppe Boriani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0453.
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The diagnosis of first-degree and third-degree atrioventricular (AV) block is straightforward but that of second-degree AV block is more involved. Type I block and type II second-degree AV block are electrocardiographic patterns that refer to the behaviour of the PR intervals (in sinus rhythm) in sequences (with at least two consecutive conducted PR intervals) where a single P wave fails to conduct to the ventricles. Type I second-degree AV block describes visible, differing, and generally decremental AV conduction. Type II second-degree AV block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. The diagnosis of type II block requires a stable sinus rate, an important criterion because a vagal surge (generally benign) can cause simultaneous sinus slowing and AV nodal block, which can resemble type II block. The diagnosis of type II block cannot be established if the first post-block P wave is followed by a shortened PR interval or by an undiscernible P wave. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute myocardial infarction is infranodal in 60–70% of cases. All correctly defined type II blocks are infranodal. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be AV nodal or infranodal. Concealed His bundle or ventricular extrasystoles may mimic both type I or type II block (pseudo-AV block), or both
24
Erlinge, David, and Göran Olivecrona. Diagnosis and management of ST-elevation of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0147.
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ST-elevation myocardial infarction (STEMI) is generally caused by a ruptured plaque that triggers local thrombus formation, which occludes the coronary artery. STEMI should be diagnosed rapidly, based on the combination of ST-segment elevation and symptoms of acute myocardial infarction. The main treatment objective is myocardial tissue reperfusion as quickly as possible. The preferred method of reperfusion is primary percutaneous coronary interventionif transport time is below 2 hours, and thrombolysis if longer STEMI patients with acute onset cardiogenic shock should be evaluated by echocardiography to exclude mechanical complications, such as flail mitral insufficiency, ventricular septal defect or tamponade. Secondary prevention includes aspirin, adenosine diphosphate receptor antagonists, statins, beta-blockers, angiotensin-converting enzymeinhibitors, and lifestyle changes.
25
Patent Foramen Ovale Closure for Stroke, Myocardial Infarction, Peripheral Embolism, Migraine, and Hypoxemia. Elsevier, 2020. http://dx.doi.org/10.1016/c2018-0-02016-2.
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26
Cardiac Regeneration and Repair : Volume 2: Biomaterials and Tissue Engineering. Elsevier Science & Technology, 2014.
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27
Cousins, Norman. The Healing Heart. Books on Tape, Inc., 1985.
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28
Cousins, Norman. Healing Heart. Random House Value Publishing, 1986.
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29
Cousins, Norman. The Healing Heart. Dove Entertainment Inc, 1987.
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30
(Narrator), William Conrad, ed. The Healing Heart. Media Books Audio Publishing, 1999.
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31
Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.
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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
32
Carton, James. Cardiac pathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0004.
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Congenital heart disease 40Angina pectoris 42Unstable angina 43Non-ST-elevation myocardial infarction 44ST-elevation myocardial infarction 46Left ventricular failure 48Right ventricular failure 50Valvular heart disease 51Cardiomyopathies 52Infective endocarditis 53Myocarditis 54Pericarditis 55• Most common type of congenital heart disease (CHD)....
33
White, Karen, and Lorna Barrett. A Fatal Chapter. Tantor Audio, 2015.
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34
White, Karen, and Lorna Barrett. A Fatal Chapter. Tantor Audio, 2015.
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35
Barrett, Lorna. A fatal chapter. 2015.
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36
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.
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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
37
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.
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Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
38
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
39
AlJaroudi, Wael. Risk Assessment in Acute Coronary Syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0013.
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Acute coronary syndromes (ACS) include unstable angina pectoris (UAP), non-ST elevation (NSTEMI), and ST elevation acute myocardial infarction (STEMI). Each year, more than 2 million people are hospitalized with ACS in the United States. The initial treatment has evolved over the last few decades from conservative management to early reperfusion therapy. Medical therapy has also significantly changed with the use of newer more potent antiplatelet agents, beta-blockers, angiotensin converting enzyme inhibitors, statins, and anti-anginal drugs, which have resulted in improvement of patient care and survival. There is no role for stress myocardial perfusion imaging (MPI) in the acute presentation; however, rest MPI may be used to identify the culprit lesion and risk stratify patients if injected during chest pain. In stable patients for ACS, submaximal exercise or vasodilator MPI can be performed as early as 48 hours after the event. Several gated MPI-derived variables such as left ventricular (LV) ejection fraction (EF), LV volumes, infarct size, mechanical dyssynchrony, and residual ischemic burden can risk stratify patients and provide prognostic data incremental to validated clinical risk scores such as GRACE (Global Registry of Acute Coronary Syndrome) and TIMI (Thrombolysis in Myocardial Infarction). Patients with depressed LVEF, remodeled LV, and large perfusion defects are at particularly high- risk for subsequent cardiac death or recurrent myocardial infarction. In such setting, MPI plays a pivotal role in the management of patients and guiding therapeutic decisions. The current chapter will review the clinical and MPI predictors of outcomes in patients presenting with ACS according to updated guidelines and a proposed algorithm integrating the role of MPI in guiding therapeutic decisions and management.
40
Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Therapy-related issues: cardiovascular system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735823.003.0016.
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This chapter is aimed at junior hospital pharmacists and community pharmacists and is loosely based on the British National Formulary, Chapter 2. It covers diagnosis, symptoms, and treatment management plans for a variety of cardiovascular topics including hypertension, heart failure, and angina, and additional topics that cover issues related to anticoagulation, acute coronary syndromes, ST-segment elevation myocardial infarction, and cardiopulmonary resuscitation.
41
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek, and Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0047.
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Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following:All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hoursPatients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groupsOther patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentationLow-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testingStents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settingsTriple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk
42
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek, and Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_001.
Full textAbstract:
Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following:All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hoursPatients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groupsOther patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentationLow-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testingStents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settingsTriple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk
43
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek, and Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_002.
Full textAbstract:
Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following: All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hours. Patients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groups. Other patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentation. Low-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testing. Stents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settings. Triple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk.
44
Kočka, Viktor, Steen Dalby Kristensen, William Wijns, Petr Toušek, and Petr Widimský. Percutaneous coronary interventions in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0047_update_003.
Full textAbstract:
Three different guidelines of the European Society of Cardiology cover the field of percutaneous coronary interventions. Their main recommendations are the following: All patients with an ST-segment elevation myocardial infarction should undergo immediate coronary angiography and percutaneous coronary intervention as soon as possible after the first medical contact. Thrombolysis can be used as an alternative reperfusion therapy if the time delay to primary percutaneous coronary intervention is more than 2 hours. Patients with very high-risk non-ST-segment elevation acute coronary syndromes (recurrent or ongoing chest pain, profound or dynamic electrocardiogram changes, major arrhythmias, or haemodynamic instability) should undergo urgent coronary angiography within less than 2 hours after the initial hospital admissionAll moderate- to high-risk (GRACE score >140 or at least one primary high-risk criterion) non-ST-segment elevation acute coronary syndromes patients should undergo coronary angiography before discharge; the ideal timing is within 24 hours after admission for high-risk groups, and within 72 hours for moderate-risk groups. Other patients with recurrent symptoms or at least one high-risk criterion should undergo coronary angiography within 72 hours of first presentation. Low-risk non-ST-segment elevation acute coronary syndromes may be treated conservatively, and the indication for an invasive evaluation can be done, based on the evidence of ischaemia during exercise stress testing. Stents should be used during all percutaneous coronary intervention procedures, whenever technically feasible. Second-generation drug-eluting stents do not increase stent thrombosis and can be safely used in the ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome settings. Triple pharmacotherapy, consisting of aspirin, thienopyridine antiplatelet agent, and anticoagulation with heparin or bivalirudin, should be used in all percutaneous coronary intervention procedures, with glycoprotein IIb/IIIa inhibitors added in patients with a high thrombus burden and low bleeding risk.
45
Cheng, Jerry, and David Madigan. Bayesian approaches to aspects of the Vioxx trials: Non-ignorable dropout and sequential meta-analysis. Edited by Anthony O'Hagan and Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.3.
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This article discusses Bayesian approaches to aspects of the Vioxx trials study, with a focus on non-ignorable dropout and sequential meta-analysis. It first provides a background on Vioxx, a COX-2 selective, non-steroidal anti-inflammatory drug (NSAID) approved by the FDA in May 1999 for the relief of the signs and symptoms of osteoarthritis, the management of acute pain in adults, and for the treatment of menstrual symptoms. However, Vioxx was found to cause an array of cardiovascular side-effects such as myocardial infarction, stroke, and unstable angina. As a result, Vioxx was withdrawn from the market. The article describes an approach to sequential meta-analysis in the context of Vioxx before considering dropouts in the key APPROVe study. It also presents a Bayesian approach to handling dropout and showcases the utility of Bayesian analysis in addressing multiple, challenging statistical issues and questions arising from clinical trials.
46
Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.
Full textAbstract:
Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume). Due to the higher thickness and myocardial fibrosis in patients with concentric LVH, ventricular compliance is reduced and the end-diastolic volume is small and insufficient to maintain cardiac output under varying physiological demands (diastolic dysfunction). In those with eccentric hypertrophy, tensile stress elongates myocardiocytes and increases LV end-diastolic volume. The LV walls are relatively thinner and with reduced ability to contract (systolic dysfunction). LVH prevalence increases stepwisely as renal function deteriorates and 70–80% of patients with kidney failure present with established LVH which is of the concentric type in the majority. Volume overload and severe anaemia are, on the other hand, the major drivers of eccentric LVH. Even though LVH may regress after renal transplantation, the prevalence of LVH after transplantation remains close to that found in dialysis patients and a functioning renal graft should not be seen as a guarantee of LVH regression. The vast majority of studies on cardiomyopathy in CKD are observational in nature and the number of controlled clinical trials in these patients is very small. Beta-blockers (carvedilol) and angiotensin receptors blockers improve LV performance and reduce mortality in kidney failure patients with LV dysfunction. Although current guidelines recommend implantable cardioverter-defibrillators in patients with ejection fraction less than 30%, mild to moderate symptoms of heart failure, and a life expectancy of more than 1 year, these devices are rarely offered to eligible CKD patients. Conversion to nocturnal dialysis and to frequent dialysis schedules produces a marked improvement in LVH in patients on dialysis. More frequent and/or longer dialysis are recommended in dialysis patients with asymptomatic or symptomatic LV disorders if the organizational and financial resources are available.
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Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.
Full textAbstract:
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.
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King, Stephen. Night Shift. Book Club Associates, 1991.
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King, Stephen. Nachtschicht. Bastei-Lübbe, 1988.
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King, Stephen. Nachtschicht. Kurzgeschichten. Lübbe, 2002.
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