Deepak Thatai

Current Guidelines for the Treatment of Patients with Rheumatic Fever

Rheumatic fever is a multisystem inflammatory disease that occurs as a delayed sequelae to group A streptococcal pharyngitis. The important clinical manifestations are migratory polyarthritis, carditis, chorea, subcutaneous nodules and erythema marginatum occurring in varying combinations. The pathogenesis of this disorder remains elusive: an antigenic mimicry hypothesis best explains the affliction of various organ systems after a lag period following pharyngeal infection. In its classic milder form, the disorder is largely self-limited and resolves without sequelae, but carditis may be fatal in severe forms of the disease. Chronic and progressive damage to the heart valves leads to the most important public health manifestations of the disease. Anti-inflammatory agents provide dramatic clinical improvement, but do not prevent the subsequent development of rheumatic heart disease. The role of corticosteroids in treatment of carditis is uncertain and controlled studies have failed to demonstrate improved long term prognosis. Chorea, once considered a benign self-limited disease, is now felt to require more aggressive treatment, in particular with sedatives. Prevention of first and subsequent attacks of rheumatic fever is the mainstay in the limited arsenal available to alter the natural history of this disease.

Clinico-pathological evaluation of restrictive cardiomyopathy (endomyocardial fibrosis and idiopathic restrictive cardiomyopathy) in India

Restrictive heart disease is characterized by impairment of ventricular filling during diastole with preserved systolic function. The clinical and histopathological profile on endomyocardial biopsy of a cohort of patients with restrictive cardiomyopathy (RCM) is presented.

Role of the renin-angiotensin-aldosterone system in diastolic heart failure: Potential for pharmacologic intervention

Congestive heart failure (CHF) is a major public health problem that results in tremendous economic burden. Diastolic heart failure (DHF) forms an important subset with increasing incidence and prevalence. There are widely variable estimates of the prevalence, ranging from 13% to 74% of all CHF presentations, and this is predominantly a result of a lack of uniform criteria for establishing a diagnosis. New developments in management of DHF have lagged behind those for systolic heart failure (SHF), for which numerous new therapeutic and device strategies have been instituted. The renin-angiotensin-aldosterone system (RAAS) plays an important role in the pathophysiology of both SHF as well as DHF. The beneficial role of ACE inhibitors as well as aldosterone antagonists in SHF has been well established. Because of its unique role of the RAAS in establishing fibrosis at a molecular level, RAAS blockade provides an opportunity to expand the therapeutic options for DHF. Thus far, in patients with primary DHF only the angiotensin receptor type 1 antagonist candesartan has been reported to decrease morbidity and probably mortality. Large, ongoing randomized trials including TOPCAT (Trial of Aldosterone Antagonist Therapy in Adults with Preserved Ejection Fraction Congestive Heart) and the I-PRESERVE (Irbesartan in Heart Failure with Preserved Systolic Function) are currently underway to establish the role of aldosterone antagonists in patients with DHF.

Cocaine-Induced Chest Pain and β-Blockade : An Inner City Experience

BackgroundCocaine is the most common illicit drug used in patients presenting with chest pain to emergency departments. Data on β-blockers in cocaine-related chest pain syndrome are sparse. We sought out to study the causal and detrimental effects of β-blockers in cocaine-related chest pain in a large inner city cohort of patients. Methods and ResultsAll patients presenting to a large inner city emergency department with chest pain, with positive urine drug screen for cocaine were included. The group comprised predominantly young (mean age 46.8 ± 8.2 years), African American (90.6%) males (73.4%). Evidence of myocardial infarction in the form of elevation of troponin-I was noted in 7.3%. Evidence of myonecrosis (MN) was significantly more likely in those who were taking β-blockers at presentation as compared with those who were not (14% versus 4.4%, P < 0.01). In the absence of prospective controlled data, our observational findings seem to suggest that routine initiation or continuation or of β-blockers after admission increased the likelihood of developing MN (23.3% versus 10.7%, P < 0.01) during the course of hospitalization. ConclusionsMN as reflected by elevation of cardiac biomarkers is uncommon in patients presenting with cocaine-related chest pain. Preexisting use of β-blockers seems to render a higher risk of myocardial injury in patients presenting with cocaine-related chest pain. In addition initiation or continuation of β-blockers during hospitalization should be discouraged.

Spectrum of electrocardiographic and angiographic coronary artery disease findings in patients with cocaine-associated myocardial infarction

BackgroundCocaine is the most common abused drug in patients presenting to the emergency room with chest pain and frequently leads to cardiac catheterization procedure. The extent of severity underlying coronary artery disease (CAD) in this subgroup of patients has not been well defined. This study set out to define the coronary anatomy as well as the extent of CAD in patients with cocaine-associated myocardial infarction (MI) and correlate that to the presenting electrocardiogram (ECG). MethodsNinety-seven consecutive patients with documented MI and positive urine drug screen for cocaine metabolites were included in the study. Demographic, clinical, ECG and coronary angiography variables were collected. ResultsST elevation MI was encountered in 32% of the patients. Other ECG findings included ST segment depression, T-wave inversion, left ventricular hypertrophy, conduction blocks and/or old MI in more than 80% of cases. Of the total of 66 patients who underwent angiography, 82% had obstructive CAD, with single-vessel disease being the most frequent finding. None of these presenting ECG findings correlated with angiographic location or severity of obstructive CAD. In nearly one-fifth of the patients, troponin elevation suggestive of cardiac myonecrosis occurred in the absence of ECG findings or angiographic coronary disease. ConclusionThe majority of patients with cocaine-associated MI have obstructive CAD with predominant single-vessel disease. Although ECG abnormalities are frequently encountered, they are of limited diagnostic value in the clinical decision making.

Pharmacological prevention of thromboembolism in patients with left ventricular dysfunction.

Chronic left ventricular systolic dysfunction is a well recognized problem with an increasingly significant impact on healthcare in the form of congestive heart failure (CHF). Advances in medicine have led to improved survival after myocardial infarction (MI) and as a result, an increased prevalence of left ventricular systolic dysfunction. An increased incidence of thromboembolism, especially stroke, in patients with left ventricular systolic dysfunction is also well recognized. Pharmacological strategies to prevent stroke have been proposed in numerous studies. For example, anticoagulation in patients with atrial fibrillation and heart failure has been shown to reduce mortality rates and the incidence of stroke; however, its role in patients with left ventricular dysfunction and normal sinus rhythm is unclear and utilization of anticoagulation in these patients varies widely. The role of aspirin to prevent thromboembolism in patients with CHF is controversial. The relatively new pharmacological agent ximelagatran, which has an advantage of unmonitored oral administration has the potential to change the anticoagulation strategy in patients with heart failure. Important trials to define optimal therapy for reducing the risk of thromboembolism and death in patients with left ventricular systolic dysfunction and sinus rhythm include the recently reported WATCH (Warfarin and Antiplatelet Therapy in Chronic Heart failure) trial and the WARCEF (Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction) trial, which is currently underway. The WATCH trial failed to outline significant differences between aspirin (acetylsalicylic acid), warfarin, and clopidogrel in the primary composite endpoint of all-cause mortality, nonfatal MI, and nonfatal stroke. Combined data from WATCH and WARCEF may provide sufficient statistical power to clarify outcomes such as stroke and death in patients with reduced cardiac ejection fraction. The pooled data may also help define optimal preventative measures for thromboembolism in patients with left ventricular systolic dysfunction and sinus rhythm.

Critical appraisal of left ventricular function assessment by the automated border detection method on echocardiography.: Is it good enough?

Many studies have attempted to validate the echocardiographic automated border detection (ABD) method for assessing left ventricular ejection fraction (LVEF) by comparing it with various echocardiographic and non-echocardiographic standards. The main basis of assessing its accuracy has been the coefficient of correlation. The fallacy of using coefficient of correlation for assessing agreement between two methods of measurement has been well emphasized in the literature. In the present study we used the Bland and Altman test for testing the accuracy of the ABD method. We compared the ABD method for LVEF assessment with the manual edge detection technique on echocardiography and with radionuclide ventriculography in 34 patients. The majority of patients (76%) had regional wall motion abnormality. The ABD method could be adequately performed in 25 (74%) patients. LVEF was significantly underestimated by the ABD method with very wide limits of agreement when compared with radionuclide ventriculography and the manual edge detection technique (-9.2+/-21.7 and -2.7+/-18.4 respectively, mean error+/-2 standard deviations). Stated simply, the ABD method could overestimate LVEF by 12.5 and 15.7 or underestimate by 30.9 and 21.1 when compared with radionuclide ventriculography and manual edge detection technique, respectively. This large error is by no means acceptable for clinical purposes. It is concluded that at the present stage, the ABD method cannot replace radionuclide ventriculography and manual edge detection technique for assessing LVEF.

Percutaneous transvenous mitral commissurotomy for rheumatic mitral stenosis with impaired left ventricular function: an echocardiographic follow-up study.

Sixty consecutive patients of rheumatic mitral stenosis who underwent percutaneous transvenous mitral commissurotomy were evaluated and followed up for 3 months in order to study the effect of the procedure on left ventricular ejection fraction and to elucidate the pathophysiology of impaired left ventricular function. The response in 16 patients (26.7%) with left ventricular dysfunction (ejection fraction less than 50%) was compared to that in 44 patients with normal left ventricular ejection fraction. Patients with left ventricular dysfunction had relatively larger left ventricular end-diastolic (84 +/- 15 vs. 76 +/- 14 ml) and end-systolic (45 +/- 11.5 vs. 35 +/- 12 ml) volumes. Percutaneous transvenous mitral commissurotomy was successful in all patients. Mitral valve area increased in all patients, from 0.8 +/- 0.2 cm2 to 1.82 +/- 0.37 cm2. After commissurotomy there was a trend towards increase of the left ventricle end-diastolic volumes in both groups of patients. Left ventricular ejection fraction also marginally increased in both groups. A reduced left ventricular compliance due to thickened and fibrotic mitral valve apparatus and excessive afterload due to increased systemic vascular resistance because of low output are possible mechanisms for left ventricular dysfunction in patients with mitral stenosis.

QT dispersion at rest and during adenosine stress myocardial perfusion imaging correlation with Myocardial Jeopardy Score.

The usefulness of QT dispersion (QTd) during adenosine myocardial perfusion imaging (MPI) to predict severity of coronary artery disease (CAD) has not been studied.