Academic literature on the topic '"cardiology", "coronary physiology", "acute myocardial infarction", "coronary microvascular dysfunction"'

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.

Takotsubo cardiomyopathy (TC), otherwise known as stress cardiomyopathy, is characterised by acute, transient left ventricular systolic dysfunction with apical ballooning in the absence of obstructive epicardial coronary stenosis. The presentation of TC mimics that of acute myocardial infarction. More recently there has been a shift towards thinking of TC as a ‘microvascular acute coronary syndrome’. Our case is of an 82-year-old woman who presented with TC mimicking acute anterior ST elevation myocardial infarction in the context of sepsis. Slow flow noted in the left anterior descending artery prompted us to perform coronary physiology. Her fractional flow reserve was 0.91, with an index of myocardial resistance of 117 and a coronary flow reserve of 1.6. In combination these results are indicative of microvascular coronary dysfunction in the absence of significant epicardial stenosis.

Abstract Left ventricular (LV) hypertrophy (LVH) is a growth in left myocardial mass mainly caused by increased cardiomyocyte size. LVH can be a physiological adaptation to physical exercise or a pathological condition either primary, i.e. genetic, or secondary to LV overload. Patients with both primary and secondary LVH have evidence of coronary microvascular dysfunction (CMD). The latter is mainly due to capillary rarefaction and adverse remodelling of intramural coronary arterioles due to medial wall thickening with an increased wall/lumen ratio. An important feature of this phenomenon is the diffuse nature of this remodelling, which generally affects the coronary microvessels in the whole of the left ventricle. Patients with LVH secondary to arterial hypertension can develop both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). These patients can develop HFrEF via a ‘direct pathway’ with an interval myocardial infarction and also in its absence. On the other hand, patients can develop HFpEF that can then progress to HFrEF with or without interval myocardial infarction. A similar evolution towards LV dysfunction and both HFpEF and HFrEF can occur in patients with hypertrophic cardiomyopathy, the most common genetic cardiomyopathy with a phenotype characterized by massive LVH. In this review article, we will discuss both the experimental and clinical studies explaining the mechanisms responsible for CMD in LVH as well as the evidence linking CMD with HFpEF and HFrEF.

Abstract Early mechanical reperfusion of the epicardial coronary artery by primary percutaneous coronary intervention (PCI) is the guideline-recommended treatment for ST-elevation myocardial infarction (STEMI). Successful restoration of epicardial coronary blood flow can be achieved in over 95% of PCI procedures. However, despite angiographically complete epicardial coronary artery patency, in about half of the patients perfusion to the distal coronary microvasculature is not fully restored, which is associated with increased morbidity and mortality. The exact pathophysiological mechanism of post-ischaemic coronary microvascular dysfunction (CMD) is still debated. Therefore, the current review discusses invasive and non-invasive techniques for the diagnosis and quantification of CMD in STEMI in the clinical setting as well as results from experimental in vitro and in vivo models focusing on ischaemic-, reperfusion-, and inflammatory damage to the coronary microvascular endothelial cells. Finally, we discuss future opportunities to prevent or treat CMD in STEMI patients.

Abstract The microvascular disease represents a widespread clinical entity in the general population, especially among women. The dysfunction of the microcirculation is often responsible for myocardial ischaemia and angina in the absence of significant stenosis of the epicardial district, while in other cases it can represent a contributing cause of angina even in the presence of coronary artery disease, cardiomyopathies or heart failure. The cardiovascular risk factors of people with microvascular disease are similar to those who develop epicardial atherosclerotic disease. However, the prognostic significance of microvascular disease remains a matter of debate. An element to be clarified, in fact, is whether subjects with dysfunction of the microcirculation and coronary tree without significant stenoses present an increased risk of myocardial infarction and sudden death. In recent years, several studies seem to confirm an association between microvascular disease and progression of coronary epicardial atherosclerosis. The prognosis of microvascular disease would therefore not be benign as was previously believed, but associated with an increased risk of cardiovascular events including revascularization, heart attack, and cardiac death.

Aims: Coronary microvascular dysfunction (CMD) is common in patients with non-obstructive coronary arteries but has not been described in low-risk symptomatic patients. We therefore assessed the prevalence and characteristics of CMD in low to moderate risk patients with chest pain in an emergency department. Methods and results: We used three-dimensional Rb82 cardiac positron emission tomography/computed tomography to diagnose coronary artery disease (known or new regional defect, any coronary calcification) and CMD (low coronary flow reserve without coronary artery disease) in chest pain patients after being ruled out for acute myocardial infarction. Exclusions included age 30 years or less, acute myocardial infarction, hemodynamic instability, heart failure and dialysis. Among 195 participants undergoing cardiac positron emission tomography/computed tomography, 42% had CMD, 36% had coronary artery disease and 22% had normal flows; 70% were women and 84% were obese. Patients with CMD and coronary artery disease had significantly lower coronary flow reserve than normal patients (mean coronary flow reserve 1.6 and 1.9 vs. 2.6, respectively, P<0.05). However, CMD patients were younger (mean age 51 vs. 61 years), and had fewer traditional cardiac risk factors ( P<0.05) than patients with coronary artery disease. Nearly one third (31%) of patients had a prior emergency department visit for chest pain within three years of index presentation. Women were four times as likely to have CMD as men (adjusted odds ratio 4.2; 95% confidence interval 1.8, 9.6) after controlling for age, race, hypertension, diabetes, smoking, dyslipidemia, obesity and family history of coronary artery disease. Conclusions: Despite their low-risk profile, nearly one half of symptomatic and mostly obese emergency department patients without evidence of myocardial infarction or coronary artery disease had CMD. The results could explain the high rates of return visits associated with chest pain, although their application to the general emergency department population require validation.

Takotsubo cardiomyopathy (TTC) is an acute, stress-induced cardiomyopathy with an increased prevalence in post-menopausal women. The syndrome is most frequently precipitated by an acute emotional or physical stressor and mimics acute myocardial infarction with symptoms, electrocardiogram (ECG) changes and cardiac troponin elevation that are indistinguishable from those caused by plaque rupture or coronary thrombosis. Diagnosis of TTC is made when coronary angiography reveals no obstructive coronary artery disease and the left ventricle demonstrates apical ballooning and basal hypercontractility. Other ventricular patterns have also been described. An abnormal myocardial response to the catecholamine surge from an emotional or a physical stressor is implicated in the pathophysiology, but the reasons for the high prevalence of TTC presentations in post-menopausal women are unknown. Several mechanisms including multi-vessel coronary vasospasm, endothelial and coronary microvascular dysfunction and direct catecholamine toxicity have been proposed. No specific guidelines for treatment of TTC have been established, but treatment is based on the American Heart Association/ American College of Cardiology guidelines for acute coronary syndrome/acute myocardial infarction and heart failure guidelines. In this review article, we discuss the characteristic clinical presentation of TTC and the commonly proposed mechanisms.

ObjectivesEarly detection of microvascular dysfunction after acute myocardial infarction (AMI) could identify patients at high risk of adverse clinical outcome, who may benefit from adjunctive treatment. Our objective was to compare invasively measured coronary flow reserve (CFR) and hyperaemic microvascular resistance (HMR) for their predictive power of long-term clinical outcome and cardiac magnetic resonance (CMR)-defined microvascular injury (MVI).MethodsSimultaneous intracoronary Doppler flow velocity and pressure measurements acquired immediately after revascularisation for AMI from five centres were pooled. Clinical follow-up was completed for 176 patients (mean age 60±10 years; 140(80%) male; ST-elevation myocardial infarction (STEMI) 130(74%) and non-ST-segment elevation myocardial infarction 46(26%)) with median follow-up time of 3.2 years. In 110 patients with STEMI, additional CMR was performed.ResultsThe composite end point of death and hospitalisation for heart failure occurred in 17 patients (10%). Optimal cut-off values to predict the composite end point were 1.5 for CFR and 3.0 mm Hg cm−1•s for HMR. CFR <1.5 was predictive for the composite end point (HR 3.5;95% CI 1.1 to 10.8), but not for its individual components. HMR ≥3.0 mm Hg cm−1 s was predictive for the composite end point (HR 7.0;95% CI 1.5 to 33.7) as well as both individual components. HMR had significantly greater area under the receiver operating characteristic curve for MVI than CFR. HMR remained an independent predictor of adverse clinical outcome and MVI, whereas CFR did not.ConclusionsHMR measured immediately following percutaneous coronary intervention for AMI with a cut-off value of 3.0 mm Hg cm−1 s, identifies patients with MVI who are at high risk of adverse clinical outcome. For this purpose, HMR is superior to CFR.

ST-segment elevation myocardial infarction (STEMI) is still associated with a 10% one-year mortality and up to 25% risk of heart failure. The pressure-wire index of microcirculatory resistance (IMR) may have an important role in the assessment of the downstream microcirculatory function of the IRA, providing prognostically relevant information and identifying patients at risk of suboptimal reperfusion who are eligible for additional novel therapies. However, the penetration of IMR in the clinical practice is still limited mainly because of the technical complexity of the procedure and increased costs and procedural time. Nevertheless, the implementation of a risk stratification using coronary physiology in patients with STEMI would be highly desirable to further improve the clinical outcomes. In this PhD thesis we aimed to assess the long-term prognostic implications of CMD investigated using IMR. Furthermore, we aim to develop alternative methods to simplify the assessment of CMD in the catheterization laboratory and increase the penetration of physiology in the clinical practice. The current thesis consists of five main chapters. In Chapter one we explored the long-term clinical outcome of patients with STEMI stratified according to IMR and cardiovascular magnetic resonance imaging (CMR) in the cohort of the OxAMI Study. Importantly, CMD defined by IMR>40 U or by MVO demonstrated a more than 4-fold increase in mortality, heart failure or cardiac arrest at a median follow-up of 40 months. In Chapter two, pressure-bounded coronary flow reserve (pb-CFR), an index derived using standard pressure-wire technology was compared with IMR and CFR in predicting microvascular obstruction and the extent of the infarct size at CMR imaging. Pb-CFR provided a fair prognostic stratification identifying a subgroup of patients with satisfactory myocardial reperfusion after PPCI. Nonetheless, the prognostic value of pb-CFR was inferior compared with IMR. Chapter three reports the derivation of an angiography-derived pressure-wire free index of microcirculatory resistance (IMRangio). IMRangio has been developed to overcome some of the limitations of IMR, using the Quantitative Flow Ratio (QFR) algorithm to obtain Pd and contrast frame count to estimate coronary flow. IMRangio demonstrated to be significantly correlated with invasive IMR in a prospective 3 cohort of patients with STEMI. Importantly, IMRangio was also correlated with the presence of MVO at CMR. In Chapter four, IMRangio was assessed in a prospective cohort of patients across the spectrum of acute and chronic coronary syndromes. Interestingly, IMRangio was well-correlated with IMR not only in STEMI but also in patients with NSTEMI e stable coronary syndromes. Moreover, we observed that IMRangio measured in non- hyperemic conditions (NH-IMRangio) provided good diagnostic performance in the subgroup of patients with STEMI. Chapter five reports on the long-term prognostic implications of patients with STEMI stratified according to NH-IMRangio in a retrospective analysis of the OxAMI Study. Notably, NH IMRangio demonstrated a prognostic value equivalent to invasively measured IMR. In conclusion, CMD has important prognostic implications at long-term after STEMI. IMRangio has the potential to guide additional novel additional therapies in patients undergoing PPCI. Abolishing the need for pressure-wire, IMRangio may increase the penetration of CMD assessment in the catheterization laboratory and physiology-guided additional therapies. Further additional data are needed to explore the role of IMRangio as a routine addition to diagnostic and interventional procedures in STEMI patients.