Frequency of elevated troponin I and diagnosis of acute myocardial infarction.

This study evaluated the incidence and type of acute myocardial infarction (AMI) in a consecutive population with increased troponin I (TnI). AMI has recently been redefined and subclassified. Incidence, demographic data, angiographic findings, and hospital mortality of patients with various AMI subtypes or an increased TnI in the absence of AMI have not been previously reported in a prospective study. Over a 3-month period, all patients admitted from an emergency room or from in-patient services with >1 TnI level >0.04 ng/ml were evaluated and subclassified in AMI subgroups. In-hospital or recent coronary angiograms were reviewed. In-hospital mortality was noted. Of 2,944 patients with serial TnI measurements, 728 had an increased TnI and 701 (23.8%) were evaluated. Two hundred sixteen (30.8% with increased TnI and 42.7% with "rule-out MI" on admission) met criteria for AMI. One hundred forty-three (20.4%) had type 1, 64 (9.1%) had type 2, whereas 461 (65.8%) did not meet criteria for AMI. On multivariate analysis, use of angiography, peak TnI level, hyperlipidemia, and illicit drug use were independently associated with the diagnosis of AMI. TnI of 0.28 ng/ml had a 70% sensitivity and specificity for AMI diagnosis. In conclusion, a minority admitted with increased TnI have AMI by the universal definition. Type 1 is the most common AMI and is associated with higher TnI values and these patients are more likely to undergo angiography. Type 2 AMI is often associated with illicit drug use.

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

BACKGROUND: Cocaine 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). METHODS: Ninety-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. RESULTS: ST 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. CONCLUSION: The 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.

Cardiac troponin-I: a predictor of prognosis in subarachnoid hemorrhage.

BACKGROUND: Release of cardiac biomarkers is reported in patients with subarachnoid hemorrhage (SAH). Data addressing the impact of cardiac injury on outcome in these patients is sparse. This study was conducted to ascertain the association of elevation of serum cardiac Troponin-I (cTnI) with mortality and neurological outcome in patients with SAH. METHODS: Medical records of all patients admitted with a diagnosis of SAH and at least one measured cTnI were reviewed. Demographic and clinical variables including admission neurological status were collected. Conservative and non-parametric statistics were used to assess association between cTnI and death or neurological outcome at discharge. RESULTS: The study group comprised of 83 patients with a mean age of 59 years. There was a female (60%) and African-American (60%) preponderance. At admission, the median Glasgow Coma Scale (GCS) was 9, and 47% had a severe Hunt-Hess grade (HHG) of > or =4. Elevation of cTnI was found in 31 (37%) patients and was associated with worse baseline Fisher grade (p=0.01) and neurological status: GCS score (p=0.006) and HHG (p=0.007). Patients with abnormal cTnI were more likely to die (55% vs.27%; odds ratio 1.3-8.4, p = 0.01) and had a worse GCS score (p = 0.008) and HHG (p = 0.004) on discharge. On multivariate analysis, peak cTnI (p = 0.04) and admission GCS score of <12 (p = 0.02) were independent predictors of death at discharge. CONCLUSION: Patients with subarachnoid hemorrhage and elevated cTnI are found to have worse neurological status at admission. These patients have a worse neurological outcome and in-hospital mortality.

Cocaine-induced chest pain and beta-blockade: an inner city experience.

BACKGROUND: Cocaine is the most common illicit drug used in patients presenting with chest pain to emergency departments. Data on beta-blockers in cocaine-related chest pain syndrome are sparse. We sought out to study the causal and detrimental effects of beta-blockers in cocaine-related chest pain in a large inner city cohort of patients. METHODS AND RESULTS: All 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 beta-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 beta-blockers after admission increased the likelihood of developing MN (23.3% versus 10.7%, P < 0.01) during the course of hospitalization. CONCLUSIONS: MN as reflected by elevation of cardiac biomarkers is uncommon in patients presenting with cocaine-related chest pain. Preexisting use of beta-blockers seems to render a higher risk of myocardial injury in patients presenting with cocaine-related chest pain. In addition initiation or continuation of beta-blockers during hospitalization should be discouraged.

Apical hypertrophic cardiomyopathy: potential utility of Strain imaging.

Hypertrophic cardiomyopathy (HCM) is a frequently recognized condition on echocardiography. The apical variant, also known as 'Japanese variant', is rare and often poses a diagnostic challenge. There has been a resurgence of interest in the diagnosis of HCM especially with the advent of novel imaging modalities such as strain imaging. Two-dimensional (2D) strain echocardiography calculates tissue velocities via frame-to-frame tracking of acoustic markers within the image and provides strain parameters comparable with tissue-Doppler-derived strain. We describe paradoxical apical strain (systolic lengthening) without overt apical dyskinesis (conventional imaging) in two patients with apical HCM, using 2D strain imaging. Our report highlights a novel application of 2D strain imaging that could facilitate the diagnosis of apical HCM.

Acquired coronary cameral fistula--a report of two cases.

BACKGROUND: Coronary cameral fistulas (CCF) are an uncommon clinical entity; encountered occasionally during cardiac catheterization. These fistulas most commonly result from congenital abnormalities leading to neovascularization. Other possible etiologies include trauma during surgery or coronary intervention. These fistulas usually terminate directly in a cardiac chamber, most often in the right ventricle. CASE PRESENTATION: We describe two cases of CCF where a previous coronary angiogram did not show the presence of the abnormality. Cardiac catheterization in our first patient revealed the presence of a fistula from the right coronary artery draining into the right ventricle. A coronary angiogram performed three years prior to this procedure revealed no obstructive coronary artery disease and no evidence of this fistula. In contrast our second case had an aortic valve replacement for severe aortic stenosis. A cardiac catheterization prior to the surgery revealed normal coronaries with no fistula. The patient's subsequent angiogram three years later revealed the acute marginal branch of the right coronary artery draining into the right atrium. CONCLUSION: Coronary cameral fistula is a rare clinical entity and can be acquired during an individual's lifetime. The puzzling presentation in our first patient is unique because CCF was acquired despite lack of previous instrumentation or trauma to the right coronary artery. The exact mechanism of fistula formation is unknown. However a possible hypothesis is secondary to hypoxia-induced angiogenesis, which has not been described to date.

Crack whips the heart: a review of the cardiovascular toxicity of cocaine.

Cocaine is an extremely powerful reinforcing psychostimulant with highly addictive properties. Over the last few decades, cocaine addiction has attained epidemic proportions in North America, imposing a tremendous burden on society and the health care system. The cardiovascular complications of cocaine abuse are adrenergic mediated and range from cocaine-associated acute coronary syndromes to aortic dissection and sudden cardiac death. Concomitant alcohol and cigarette smoking exacerbate the cardiotoxicity of cocaine. This contemporary review discusses the spectrum of cardiac complications arising from cocaine use, operant pathophysiologic mechanisms and controversies surrounding the pharmacotherapy of cocaine-associated acute coronary syndromes.

Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease.

Spontaneous coronary artery spasm is an important cause of morbidity both in patients with atherosclerotic coronary artery disease and in those with Prinzmetal's angina. Coronary vasospasm tends to occur in focal areas in the coronary tree and can be readily induced by the use of various agents. Spontaneous severe multivessel spasm, mimicking severe obstructive coronary artery disease, has been infrequently described. The therapeutic dilemma in such a clinical situation is highlighted in our current case where an unnecessary coronary artery bypass graft surgery (CABG) was performed due to the lack of clinical suspicion of spasm. This patient presented 5 years after triple-vessel CABG with an episode of rest angina, and was initially found to have severe obstruction of all three native coronary arteries with patent grafts to the right coronary and left anterior descending arteries. After nitroglycerin injection, all three native vessels appeared large and normal. This report raises the question of whether the routine use of intracoronary nitroglycerin, largely abandoned over the past 20 years, should be revisited, at least for certain patient populations such as those with rest angina.

Thromboembolic complications of left ventricular noncompaction: case report and brief review of the literature.

Left ventricular noncompaction (LVNC) is a rare condition that is believed to represent an arrest in endomyocardial morphogenesis. This entity may be complicated by the development of mural thrombi and embolic events, however data on the associated thromboembolic risk is variable and poorly defined. We describe 2 cases of LVNC in African American patients presenting with thromboembolic manifestations and briefly review the available literature relevant to this complication.

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.

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.

Common errors in computer electrocardiogram interpretation.

OBJECTIVE: The aim of the study was to determine the frequency and nature of errors in computer electrocardiogram (ECG) reading. METHODS: The ECGs were collected in the tertiary care VA Hospital from both inpatients and outpatients. They were read by the electrocardiograph built-in computer software, and then reread by two cardiologists. Statistical analysis was performed using sensitivity, specificity, positive and negative predicted value to analyze the data. An error index was formulated as indicator of diagnostic accuracy. RESULTS: Out of 2072 ECGs, 776 (37.5%) were normal, and 1296 (62.5%) were abnormal. In 9.9% of all ECGs and in 15.9% of abnormal ECGs there were significant disagreements between the computer and cardiologists. The errors in diagnosis of arrhythmia, conduction disorders and electronic pacemakers accounted for 178 cases, or 86.4% of all errors. The rest was represented by misdetection of chamber enlargement (7 cases, 3.4%), misdiagnosis of ischemia and acute myocardial infarction (16 cases, 7.8%), and lead misplacement (5 cases, 2.4%). CONCLUSIONS: The most frequent errors in computer ECG interpretation are related to arrhythmias, conduction disorders, and electronic pacemakers. Computer ECG diagnosis of life threatening conditions e.g. acute myocardial infarction or high degree AV blocks are frequently not accurate (40.7% and 75.0% errors, respectively). Improvement in the diagnostic algorithms should focus on these areas. Error index is a convenient and informative tool for evaluation of diagnostic accuracy.

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

BACKGROUND: 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. METHODOLOGY: The medical records of patients presenting with heart failure with systemic congestion, subsequently diagnosed as restrictive heart disease after evaluation including cardiac catheterisation, were studied retrospectively to determine the clinical spectrum of restrictive cardiomyopathy. The diagnosis of RCM was made, based on systemic congestion with dilated atria and near normal ventricular size and function. Only patients who had an endomyocardial biopsy were included in the study. Patients with chronic constrictive pericarditis and secondary restrictive heart disease mainly amyloidosis were excluded from the study. RESULTS: All 52 patients had heart failure with normal or near normal left ventricular size and function. Based on right and left ventricle angiography, patients were classified into two groups. Group I with findings suggestive of EMF (n=30) and Group II no evidence of EMF on angiography i.e. 'idiopathic RCM' (IRCM) (n=22). Baseline characteristics were similar in the two groups. Echocardiography revealed typical features of endomyocardial fibrosis in Group I patients, with apical obliteration of right and left ventricular apices. Group II patients had no apex obliteration (except in four patients, who were misclassified and in whom angiography did not show apex obliteration). The Group II patients had features of IRCM in the form of normal left and right ventricular size and function with restrictive features of doppler filling along with dilated left and right atria. Angiocardiography in EMF patients showed isolated RV involvement in only two patients. In the remaining 28 patients, the obliterative changes were biventricular with RV involvement more severe than LV involvement. Angiographic findings in Group II (IRCM) patients were unremarkable with preservation of normal trabecular pattern and absence of obliterative changes. Mild atrioventricular regurgitation was present in 10/22 patients. Histopathological examination revealed that endocardial thickening was more common (77% vs. 23%) in EMF patients. The presence of myocyte hypertrophy (70-80%), myocytolysis (40-50%) and interstitial fibrosis (46-56%) were similar in both groups. CONCLUSIONS: The majority of our patients had biventricular EMF. A significant number of patients had clinical hemodynamic features of restrictive heart disease but no evidence of EMF on angiography. These IRCM patients had similar clinical profiles to EMF but on endomyocardial biopsy the endocardial thickening was minimal and seen in few patients (5/22).