Myocardial Perfusion PET for the Detection and Reporting of Coronary Microvascular Dysfunction: A JACC: Cardiovascular Imaging Expert Panel Statement.

Angina pectoris and dyspnea in patients with normal or nonobstructive coronary vessels remains a diagnostic challenge. Invasive coronary angiography may identify up to 60% of patients with nonobstructive coronary artery disease (CAD), of whom nearly two-thirds may, in fact, have coronary microvascular dysfunction (CMD) that may account for their symptoms. Positron emission tomography (PET) determined absolute quantitative myocardial blood flow (MBF) at rest and during hyperemic vasodilation with subsequent derivation of myocardial flow reserve (MFR) affords the noninvasive detection and delineation of CMD. Individualized or intensified medical therapies with nitrates, calcium-channel blockers, statins, angiotensin-converting enzyme inhibitors, angiotensin II type 1-receptor blockers, beta-blockers, ivabradine, or ranolazine may improve symptoms, quality of life, and outcome in these patients. Standardized diagnosis and reporting criteria for ischemic symptoms caused by CMD are critical for optimized and individualized treatment decisions in such patients. In this respect, it was proposed by the cardiovascular council leadership of the Society of Nuclear Medicine and Molecular Imaging to convene thoughtful leaders from around the world to serve as an independent expert panel to develop standardized diagnosis, nomenclature and nosology, and cardiac PET reporting criteria for CMD. This consensus document aims to provide an overview of the pathophysiology and clinical evidence of CMD, its invasive and noninvasive assessment, standardization of PET-determined MBFs and MFR into "classical" (predominantly related to hyperemic MBFs) and "endogen" (predominantly related to resting MBF) normal coronary microvascular function or CMD that may be critical for diagnosis of microvascular angina, subsequent patient care, and outcome of clinical CMD trials.

Relation of Heavy Alcohol Consumption to QTc Interval Prolongation.

Until now, few studies have examined QT intervals in subjects who consume alcohol. We performed this study to evaluate the associations between alcohol consumption and the QTc interval based on a general population. A total of 11,269 adults were examined using a multistage cluster sampling method to select a representative sample of subjects aged ≥35 years. Participants were asked to provide information about their alcohol consumption, and all participants received electrocardiograms and echocardiograms. A prolonged QTc interval was defined according to the national guidelines, which specify thresholds of ≥460 ms in women and ≥450 ms in men. Patients were divided into 3 categories, based on the amount of alcohol they consumed: heavy drinkers (>15 g/day for women and >30 g/day for men), moderate drinkers (≤15 g/day for women and ≤30 g/day for men), and nondrinkers (0 g/day). The results showed that the heavy drinkers had longer QTc intervals than did the nondrinkers. Multivariate logistic regression analyses revealed that men who were heavy drinkers had approximately 1.4-fold higher odds of having a prolonged QTc interval (odds ratio 1.431, 95% confidence interval [CI] 1.033 to 1.982, p = 0.031) than nondrinkers; in women, heavy drinkers had ∼2.3-fold higher odds of having a prolonged QTc interval (odds ratio 2.344, 95% CI 1.202 to 4.571, p = 0.012) than nondrinkers. Neither men nor women who were moderate drinkers exhibited a significant increase in risk for prolonged QTc interval. In conclusion, heavy alcohol consumption was found to be a risk factor for a prolonged QTc interval.

Comparison of Clinical Features in Blacks Versus Whites With Hypertrophic Cardiomyopathy.

To date, there has not been a large systematic examination of the hypertrophic cardiomyopathy (HC) phenotype in blacks versus whites. In this study, we investigate differences in presentation of HC between blacks and whites. We included 441 consecutive patients with HC seen at the Johns Hopkins HC clinic in the period from February 2005 to June 2012. We compared 76 blacks for clinical presentation, electrocardiogram, exercise capacity, left ventricular morphology, and hemodynamics by echocardiography to 365 whites. Black patients with HC more often presented with abnormal electrocardiogram (93% vs 80%, p = 0.009), driven by a significant difference in repolarization abnormalities (79% vs 56%, p <0.001). Apical hypertrophy was more common in blacks (26% vs 9%, p <0.001); however, blacks had less severe systolic anterior movement of the mitral valve and had significantly lower left ventricular outflow tract gradients at rest (9 mm Hg; interquartile range [IQR] 7 to 19 vs 16 mm Hg; IQR 8 to 40, p <0.001) and during provocation (36 mm Hg; IQR 16 to 77 vs 59 mm Hg; IQR 26 to 110, p = 0.002). Despite the nonobstructive pathophysiology, blacks had lower exercise capacity (adjusted difference 1.45 metabolic equivalents [0.45 to 2.45], p = 0.005). In conclusion, blacks have an HC phenotype characterized by lower prevalence of the well-recognized echocardiographic features of HC such as systolic anterior movement of the mitral valve and left ventricular outflow tract obstruction and display worse exercise capacity.