Neurologic complications of cardiomyopathies and other myocardial disorders.

Cardiomyopathies have a variety of causes: infectious, genetic, valvular heart disease, coronary artery disease, hypertension, and tachycardias. All can result in myocardial dysfunction and often congestive heart failure. The main interaction between a diagnosis of heart disease and the brain is via embolic stroke. The focus here is on myocardial dysfunction. Thrombus is associated with myocardial dysfunction and depressed left ventricular ejection fractions. Reduced left ventricular ejection fractions and mural thrombus are associated with embolic strokes. Atrial fibrillation is a primary source of thrombi. Anticoagulation can significantly reduce the incidence of thrombotic problems. Patent foramen ovale has created interest in those patients with cryptogenic strokes. Cryptogenic strokes are associated with patent foramen ovales, although not all cryptogenic strokes are associated with paradoxical emboli. Clinically silent cerebral infarctions occur in patients with dilated cardiomyopathy as detected by multidetector computed tomography or magnetic resonance imaging studies. Left ventricular dysfunction from cardiomyopathies is associated with mural thrombi, but the prevalence of embolic stroke varies widely from 3% to 50%; as many as half of embolic strokes are related to atrial fibrillation. Nonvalvular atrial fibrillation can increase the risk of stroke by a factor four to seven times when compared to normal sinus rhythm. Stroke risks and bleeding risks with anticoagulation can be estimated by scores. Genetic abnormalities are increasing in importance in helping to find the etiology and inheritance of some dilated cardiomyopathies. Careful clinical evaluation remains important.

Femoral angiogram prior to arteriotomy closure device does not reduce vascular complications in patients undergoing cardiac catheterization.

OBJECTIVES: To compare the efficacy of achieving hemostasis without vascular access site complications (VCs) in patients who did not undergo femoral angiogram (FA) prior to arteriotomy closure device (ACD) placement. BACKGROUND: Following coronary angiogram/percutaneous coronary intervention (CA/PCI), VCs increase morbidity and mortality. Previous studies in which an FA was highly recommended but not mandatory suggest that a predictor of VC is ACD use. METHODS: We retrospectively identified consecutive patients who underwent CA/PCI and attempted ACD deployment at our institution over a three-year period. These patients' medical and procedural records, angiogram films, and subsequent hospitalization records were reviewed to identify predetermined clinical outcomes. RESULTS: One thousand four hundred and twenty-two patients underwent CA/PCI from the transfemoral approach with ACD deployment. Seven hundred and eight (49.8%) patients did not undergo FA prior to ACD deployment. The use of ACD without FA guidance was not associated with an increased rate of combined measured clinical end-point; immediate ACD failure; retroperitoneal bleed; TIMI minor bleed; infectious complications; need for surgical intervention; or mortality (5.3 vs. 4.9; 2.7% vs. 2.2%; 1.4% vs. 0.9%; 0.5% vs. 0.4%; 0% vs. 0%; 0.1% vs. 0.1%; 0% vs. 0%, respectively, P = NS). CONCLUSION: We found no evidence that performing an FA prior to ACD placement as recommended by the manufacturer had any influence on the clinical success rate of ACD placement or rates of VCs. Therefore, ACD use without FA guidance in patients undergoing CA/PCI is an equally safe and effective method in successfully obtaining hemostasis without an increased risk of VCs.

A transfusion-related acute myocardial injury.

It is not uncommon for patients to have adverse reactions during or after blood transfusions, as they occur in 1%-6% of all blood transfusions. Although many of the reactions are clinically insignificant, a small subset of adverse reactions can lead to serious illness and even death. The authors describe a healthy young man who exhibited an acute pulmonary injury reaction to a blood product transfusion. However, he also suffered significant myocardial insult, as documented by decreased left ventricular ejection fraction and a significant rise in cardiac biomarkers. Based on current understanding of the pathophysiologic mechanisms in transfusion-related acute lung injury, the authors hypothesized that coronary endothelial injury may have caused microvascular ischemia or have induced acute myocarditis. Empiric treatment with steroids and a beta blocker resulted in improved left ventricular function in our patient.

Association of mild transient elevation of troponin I levels with increased mortality and major cardiovascular events in the general patient population.

CONTEXT: The prognostic value of mild elevation of cardiac-specific troponin I (cTnI) levels is poorly defined, which can make interpretation of such an elevation difficult. OBJECTIVE: To study the prognostic value of transient mild elevation of cTnI levels in the hospitalized patient population. DESIGN: We performed a case-control study that compared the outcome of patients hospitalized for any cause with at least 2 subsequent transient cTnI measurements of 0.1 ng/mL or higher and less than 1.5 ng/mL with matched controls with cTnI levels less than 0.1 ng/mL. A cohort of 118 patients (mean +/- SD age, 67.4 +/- 14.0 years; 35.6% men) was followed up for an average +/- SD of 11.9 +/- 7.9 months. Seventy-one cases were matched with 37 controls in terms of demographics, coronary artery disease risk factors, and reason for admission. End points were all-cause mortality and major cardiovascular end points, including cardiovascular mortality, myocardial infarction, and revascularization. RESULTS: The total event rate was significantly increased in the case group compared with the control group at 12, 6, and 3 months (62.0% vs 24.3%, 59.2% vs 16.2%, and 47.9% vs 5.4%, respectively; P < .001). At 12, 6, and 3 months, the cases had a significant increase in all-cause mortality (43.7% vs 16.2%, 40.8% vs 8.1%, and 33.8% vs 0.0%, respectively; P = .005) and major cardiovascular end points (26.8% vs 8.1%, 26.8% vs 8.1%, and 21.1% vs 5.4%, respectively; P = .02) compared with controls. CONCLUSION: Transient mild elevation of cTnI levels in hospitalized patients is associated with an increase in all-cause mortality and major cardiovascular complications. Such elevations of cTnI levels can be considered a marker for both all-cause and cardiovascular morbidity and mortality.

Antiplatelet agents: current drugs and future trends.

Antiplatelet drugs in clinical use are discussed in terms of their mechanisms of action and the relevancy of that to the physiology of platelets and the pathophysiology of arterial thrombosis. Current clinical usage is outlined in detail for each drug. Experimental antiplatelet drugs also are discussed.