Effect of intracoronary nicardipine on cardiac enzymes after elective percutaneous coronary intervention.

BACKGROUND: Elevation in cardiac enzymes after percutaneous coronary intervention (PCI) is common and is associated with adverse clinical outcomes. HYPOTHESIS: Administration of intracoronary nicardipine--a calcium channel blocker will reduce cardiac enzyme levels in patients undergoing elective PCI. METHODS: In a single center, prospective, double-blind placebo-controlled trial, 193 patients undergoing elective PCI (with or without stenting) for chronic stable angina and/or an abnormal stress test were randomized to receive 200 mcg of intracoronary nicardipine (n = 93) or saline solution (n = 100) prior to intervention. Cardiac enzyme levels were measured immediately and at 8 and 16 hours after the procedure. Major adverse clinical events (MACE) were assessed at 30 days and at 6 months. RESULTS: Incidence of periprocedural myonecrosis defined as elevation of troponin I levels > 1x the upper limit of normal was similar in both groups (placebo 15.4% vs drug 10.6%; P = 0.47). There was no significant difference in peak troponin I levels after PCI between the 2 groups (placebo 0.58 ng/mL +/- 1.08 ng/mL vs drug 0.97 ng/mL +/- 3.6 ng/mL; P = 0.35). Major adverse clinical events at 6 months were infrequent and not statistically different in the 2 groups (placebo 3.4% vs drug 1.2%; P = 0.52). Multivariate analysis revealed that pretreatment with nicardipine was not associated with reduction in the incidence of troponin I elevation (odds ratio [OR]: 0.54; 95% confidence interval [CI]: 0.18-1.6; P = 0.28). CONCLUSIONS: In low-risk patients undergoing elective PCI, intracoronary nicardipine administration did not produce a significant cardioprotective effect in reducing postprocedural cardiac enzymes leakage.

Evolving clinical application of cardiac MRI.

Over the past decade, cardiac magnetic resonance imaging (MRI) has emerged as a new technology representing the next major advance in noninvasive cardiac imaging. It provides unique and accurate data representative of cardiac structure, function, and perfusion at both the gross anatomical and myocardial levels. Cardiac MRI proves to be highly accurate and reproducible in many challenging areas in clinical cardiology, including diagnosis of constrictive pericarditis, differentiation of ischemic from dilated cardiomyopathy, confirmation of the diagnosis of myocarditis, and definition and quantification of myocardial viability. As compelling studies support its clinical utility, the evolution of cardiac MRI is gaining speed. In many cases, such as the diagnosis of anomalous origin of the coronary arteries, it is the gold standard diagnostic technique.

Transient left ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link?

We describe a patient who developed acute chest pain after using cocaine and had ST-segment elevation in the anterior leads on electrocardiography with mild elevation of cardiac enzymes. Cardiac catheterization showed normal coronary arteries with no coronary vasospasm. Left ventricular angiography revealed typical ballooning of the left ventricular apex during systole with an estimated left ventricular ejection fraction of 25%. The symptoms improved during the next few hours, and follow-up echocardiography 4 days later showed complete resolution of the left ventricular dysfunction. Transient left ventricular apical ballooning (LVAB) was diagnosed. To our knowledge, LVAB (also known as Takotsubo cardiomyopathy or "broken heart syndrome") has not been reported previously in association with cocaine use. We discuss the possible pathophysiologic link between LVAB and cocaine-induced cardiotoxicity.

From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease.

Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivascular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myocyte hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.

The no-reflow phenomenon: epidemiology, pathophysiology, and therapeutic approach.

Over the past 20 years, advances in the management of ST segment elevation myocardial infarction have focused on the rapid achievement of patency in the infarct-related artery. The limitation of this therapeutic strategy has been exposed with the development of diagnostic techniques to assess coronary microcirculation, including myocardial contrast echo, magnetic resonance imaging, myocardial perfusion grading, and the coronary flow wire. These methods have expanded our ability to understand and recognize the no-reflow phenomenon, which describes the absence of tissue perfusion despite epicardial coronary artery patency and flow. Although the mechanisms responsible for the development of no reflow are not fully understood, the end result is microvascular damage produced by microvascular obstruction or reperfusion injury. Ideally, early recognition of the no-reflow phenomenon should provide an opportunity for therapeutic intervention designed to augment tissue perfusion and maintain the viability of myocardium at risk. A number of pharmacologic agents are being used in conjunction with percutaneous transluminal coronary angioplasty in an attempt to improve microvascular perfusion. These include IIb/IIIa receptor antagonists, adenosine, verapamil, and the experimental agent nicorandil. In the new millennium, the emphasis of reperfusion therapy is being shifted downstream from its exclusive focus on the epicardial artery to assuring normal blood flow at the tissue level. This article will review the epidemiology, pathophysiology, and therapeutic approach to this vexing clinical problem.