Usman Javed

Effects of Cigarette Smoke Exposure on Clot Dynamics and Fibrin Structure An Ex Vivo Investigation

Objectives—The purpose of this study was to examine the effect of cigarette smoke exposure (CSE) on clot dynamics and fibrin architecture and to isolate the relative contribution of platelets and fibrinogen to clot dynamics. Methods and Results—From young healthy males smokers (n=34) and nonsmokers (n=34) a baseline blood was drawn, and smokers had another blood draw after smoking 2 regular cigarettes. Using thromboelastography (TEG) the degree of platelet-fibrin interaction was measured. In additional experiments, abciximab (20 &mgr;g/mL) was added to the smokers samples (n=27) to reduce the effects of platelet function from the TEG parameters. The maximum clot strength (G) obtained with abciximab measured mainly the contribution of fibrinogen to clot strength (GF). By subtracting GF from G, the contribution of platelets to clot strength (GP) was presumed. A significant difference was found for all TEG parameters between nonsmokers versus postsmoking and pre- versus postsmoking samples. Postsmoking both GF and GP were significantly higher as compared to presmoking. On electron microscopy and turbidity analysis, postsmoking fibrin clots were significantly different compared to presmoking and nonsmoking samples. Conclusions—Acute CSE changes clot dynamics and alters fibrin architecture. Both functional changes in fibrinogen and platelets appear to contribute to heightened thrombogenicity after acute CSE.

Angiographic correlates in type 1 and 2 MI by the universal definition.

In the 1980s, the angiographic morphology of culprit lesions in unstable angina and acute myocardial infarction (AMI) was described distinct from that seen in stable angina ([1,2][1]). These lesions were originally designated as “type 2 eccentric” and later on as “complex lesions.” They were

Beta-adrenergic blockers for chronic heart failure.

Systolic dysfunction and heart failure are major public health problems associated with a significant risk of morbidity and mortality. During the past 2 decades, considerable progress has been made in defining the underlying pathophysiology and the appropriate therapies in heart failure. In patients with chronic heart failure (CHF), sustained sympathetic overactivation leads to down-regulation of beta receptors and uncoupling of the receptors from adenylate cyclase. The clear understanding of the pivotal role of sympathetic overactivation in CHF has led to the evaluation of β- blocker therapy in CHF. A number of large randomized clinical trials have been conducted with a variety of β-blockers, and although most of them have shown benefit, there have been differing findings with different molecules. β-blockers are now considered part of the standard therapy for all patients with symptomatic CHF. Despite the strong evidence supporting their use, β-blockers continue to be underutilized in CHF.

Angiotensin Receptor Blockers: Novel Role in High-Risk Patients

The identification of patients at high risk for cardiovascular events is imperative in the reduction of cardiovascular mortality and morbidity. Although coronary artery disease, peripheral arterial disease, cerebrovascular disease, hypertension, and diabetes mellitus contribute to the risk of developing cardiovascular events, we are now faced with emerging fronts because of an increase in life expectancy and the epidemic of hypertension, obesity, metabolic syndrome, and diabetes. Recent data emphasize the beneficial role of renin-angiotensin-aldosterone system (RAAS) blockers. This article addresses the role of RAAS activation in the high-risk metabolic milieu and the role of angiotensin receptor blockers in targeting and inhibiting the RAAS for cardiovascular protection.

Statins in heart failure.

This article reviews the results from several recent reports describing the safety and efficacy of statin therapy in the setting of heart failure. It additionally discusses the ongoing controversy regarding the lipid paradox and possible mechanisms responsible for potential benefit of statin therapy in heart failure.

Evaluation of the Association between Compensated Hepatitis C Infectivity and Endothelial Dysfunction, Using Flow-Mediated Vasodilatation of the Brachial Artery

Background and Aim: We prospectively investigated, using sonographic methods, whether hepatitis C infection in compensated patients is related to endothelial dysfunction of the brachial artery, a potential indicator of subclinical atherosclerosis. Methods: Brachial artery flow-mediated dilatation (FMD) was used as a noninvasive test to measure the endothelial function of the brachial artery among the cases and the controls. The peak systolic velocity (PSV) and the resistive index (RI) were also measured. Multivariate statistics were used to compare the FMD, PSV, and RI in 28 cases (diagnosed with hepatitis C) and 14 healthy controls, all of whom were without cardiovascular risk factors or a history of cardiovascular disease. Results: Flow-mediated dilatation (baseline to 1 minute post-cuff inflation) was positively correlated with the patient’s body mass index (BMI) (Pearson’s r = .309, P = .025). When the BMI was accounted for using analysis of covariance (ANCOVA), there was no evidence for a significant difference between the mean FMD of the cases versus the controls (F = 0.11, P = .598). The mean FMD was 6.6% (95% confidence interval [CI], 3.1%-10.2%) among the cases and 7.3% (95% CI, 1.1%-13.6%) among the controls. Peak systolic velocity and RI (baseline to 3 minutes post-cuff inflation) were not positively correlated with BMI. The mean PSV was 0.57 m/s (95% CI, 0.51-0.66) for the cases and 0.64 m/s (95% CI, 0.56-0.72) for the controls; repeated measures analysis of variance (ANOVA) indicated no significant difference (F = 1.65, P = .208). Similarly, the mean RI was 0.87 (95% CI, 0.85-0.89) among the cases and 0.64 (95% CI, 0.82-0.88) among the controls, with no significant difference (P = .772). Conclusion: Our results show that hepatitis C positivity in compensated patients, in the absence of cardiovascular risk factors, does not appear to be independently associated with endothelial dysfunction when objectively analyzed by brachial artery flow-mediated vasodilatation.

Acute myocardial infarction and the five-chambered heart.

The case of a patient presenting with acute inferior ST‐elevation myocardial infarction is described. Emergent coronary angiography of the right coronary artery revealed what appeared to be the abrupt drainage of contrast into a large, peculiar cavity or chamber. Echocardiography and cardiac computed tomography demonstrated a giant right coronary aneurysm in the right coronary artery that gave the impression of a “fifth heart chamber.” The patient underwent successful surgical resection of the aneurysm. Diagnostic and treatment approaches to giant coronary aneurysms are discussed.