Acute ischemic heart disease and interventional cardiology: a time for pause

BACKGROUND: A major change has occurred in the last few years in the therapeutic approach to patients presenting with all forms of acute coronary syndromes. Whether or not these patients present initially to tertiary cardiac care centers, they are now routinely referred for early coronary angiography and increasingly undergo percutaneous revascularization. This practice is driven primarily by the angiographic image and technical feasibility. Concomitantly, there has been a decline in expectant or ischemia-guided medical management based on specific clinical presentation, response to initial treatment, and results of noninvasive stratification. This 'tertiarization' of acute coronary care has been fuelled by the increasing sophistication of the cardiac armamentarium, the peer-reviewed publication of clinical studies purporting to show the superiority of invasive cardiac interventions, and predominantly supporting (non-peer-reviewed) editorials, newsletters, and opinion pieces. DISCUSSION: This review presents another perspective, based on a critical reexamination of the evidence. The topics addressed are: reperfusion treatment of ST-elevation myocardial infarction; the indications for invasive intervention following thrombolysis; the role of invasive management in non-ST-elevation myocardial infarction and unstable angina; and cost-effectiveness and real world considerations. A few cases encountered in recent practice in community and tertiary hospitals are presented for illustrative purposes The numerous and far-reaching scientific, economic, and philosophical implications that are a consequence of this marked change in clinical practice as well as healthcare, decisional and conflict of interest issues are explored. SUMMARY: The weight of evidence does not support the contemporary unfocused broad use of invasive interventional procedures across the spectrum of acute coronary clinical presentations. Excessive and unselective recourse to these procedures has deleterious implications for the organization of cardiac health care and undesirable economic, scientific and intellectual consequences. It is suggested that there is need for a new equilibrium based on more refined clinical risk stratification in the treatment of patients who present with acute coronary syndromes

Acute myocardial infarction and heart failure: role of apoptosis.

Apoptosis is a key pathologic feature in acute myocardial infarction and heart failure. Experimental animal studies have show

Myocardial expression of survivin, an apoptosis inhibitor, in aging and heart failure. An experimental study in the spontaneously hypertensive rat

Background: Apoptosis plays a major role in the transition to heart failure (HF) in systemic hypertension although the underlying mechanisms are still unclear. The aim of this study was to determine the relationship between apoptosis, left ventricular remodeling, heart failure and the myocyte expression of survivin, an inhibitor of apoptosis. Methods: Spontaneously hypertensive rats (SHR) were used as a model of hypertensive cardiopathy, and Wistar Kyoto Stars rats (WKY) were used as controls. Animals were allowed to survive up to 18 months of age. The animals underwent echocardiography (EDD, ESD and FS were measured). The median section of the heart was processed for in situ end-labeling of DNA fragmentation (TUNEL) and for survivin expression by immunohistochemistry. Results: All SHR presented features of adverse cardiac remodeling. Apoptotic cells were increased in SHR compared with WKY, measured as apoptotic cells per high power field (1.08 ± 0.43 vs. 0.27 ± 0.15, P < 0.001), and as apoptotic rate (0.16 ± 0.06% vs. 0.04 ± 0.02%, P < 0.001). The incidence of apoptosis showed a positive correlation with unfavorable ventricular remodeling, assessed by echocardiogram. Survivin expression was found in all cases, but the survivin expression index was significantly lower in SHR vs. WKY (43 ± 40% vs. 86 ± 18%, respectively, P = 0.014). Moreover the survivin expression index was inversely correlated with features of adverse remodeling (i.e., Heart Weight, R = - 0.79, P < 0.001) and with apoptosis (i.e., apoptotic rate, R = - 0.52, P = 0.050). Conclusion: Survivin myocardial expression in aging SHR is associated with reduced apoptosis and more favorable cardiac remodeling. Modulation of this pathway may prove beneficial in preventing pressure overload cardiac remodeling and heart failure. © 2005 Elsevier Ireland Ltd. All rights reserved

Adjusted indirect comparison of intracoronary drug-eluting stents: evidence from a metaanalysis of randomized bare-metal-stent-controlled trials.

We pooled data from 17 studies (allocating 3048 patients to BMS and 3392 to nine different DES). Indirect head-to-head comparison of sirolimus-eluting Cypher (N=1007) vs. polymeric paclitaxel-eluting Taxus (N=959) showed nonsignificant differences in TLR [OR=0.8 (0.5–1.4), p=0.45] but significant reductions in BRR favoring Cypher [OR=0.3 (0.1–0.6), p0.50 for both TLR and BRR). Actinomycin-, mycophenolate-, and apolymeric paclitaxel-eluting stents (PES) all proved significantly worse than Cypher or Taxus for TLR or BRR.ConclusionNotwithstanding its inherent limitations, the present metaanalysis confirms the effectiveness of both Cypher and Taxus, supports the promising role of everolimus-eluting stents, and suggests the significant inferiority of most other devices. These post hoc findings, albeit intriguing, await prospective confirmatio

Role of apoptosis in pressure-overload cardiomyopathy

In the natural history of pressure overload, the hypertrophy response of the left ventricle initially normalizes wall stress and allows preservation of a normal ejection fraction. Nevertheless, patients progress gradually or suddenly from compensated hypertrophy to ventricular dilation with heart failure. Long-standing hypertrophy entails a maladaptive response, which is due to derangements inherent in the myocardium rather than to a progressive increase in the cause of pressure overload. Despite this condition being linked to major clinical consequences and an unfavourable prognosis, the cellular and molecular mechanisms in pressure-overload cardiomyopathy have not yet been established. This review discusses the available experimental and clinical evidence with respect to the role played by myocardial apoptosis in pressure-overload cardiomyopathy