1/42. The combination of risk factors for sudden death in a resuscitated elderly patient with an exceptional cause of left ventricular hypertrophy.The work-up of a previously asymptomatic 72-year-old man presenting with sudden cardiac death revealed a coarctation of the aorta as the cause of arterial hypertension, severe left ventricular hypertrophy, in combination with coronary artery disease with an apical myocardial infarction, severe autonomic dysfunction, and AV-nodal reentrant tachycardia. All these elements and their complex, probably synergistic interactions might have been involved in the development of sudden cardiac death.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
2/42. Coronary artery aneurysms, aortic dissection, and hypertension secondary to primary aldosteronism: a rare triad. A case report.Primary aldosteronism is a relatively uncommon etiology of hypertension. plasma renin activity is suppressed in the majority of the cases but not always. plasma renin activity has been associated with increased vascular injury. The occurrence of vascular complications has rarely been reported with low plasma renin activity. The authors report a case of long-standing secondary hypertension due to primary aldosteronism with coronary artery aneurysms and aortic dissection. Diagnosing is important, for therapeutic intervention can be curative.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
3/42. Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy.The 12-lead electrocardiogram (EKG), a powerful tool used in evaluating the chest pain patient, has its shortcomings. One such failing is encountered in a patient with one of the following electrocardiographic patterns: left bundle branch block (LBBB), ventricular paced rhythm (VPR), and left ventricular hypertrophy (LVH). These patterns reduce the ability of the EKG to detect acute coronary ischemic change and acute myocardial infarction (AMI). Several strategies are available to assist in the correct interpretation of these complicated electrocardiographic patterns, including a knowledge of the ST segment-T wave changes associated with these confounding patterns, performance of serial EKGs, and comparison with previous EKGs if available. This article suggests guidelines and interpretive tools for diagnosing AMI on EKG in patients with these confounding patterns.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
4/42. Echocardiographic diagnosis of sinus Valsalva aneurysm rupture in two pediatric patients.Sinus Valsalva aneurysm rupture (SVAR) is a rare cardiac abnormality that requires surgical correction when diagnosed. Previously, cardiac catheterization and angiography were thought to be necessary for its diagnosis. We present two pediatric cases of SVAR with subarterial ventricular septal defect (VSD) diagnosed noninvasively by echocardiography; surgical findings confirmed the diagnosis. In both of our cases the origin of SVAR was the right coronary sinus. The first case was ruptured into the right ventricular cavity; the second was ruptured into the right ventricular outflow tract. Continuous murmurs heard during follow-up of children with VSD must alert the physician to this pathology. Combined two-dimensional, Doppler and color-Doppler echocardiography is an accurate, noninvasive method for diagnosis of SVAR.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
5/42. Transient left ventricular aneurysm and hypertrophy accompanied by polymorphic ventricular tachycardia in a patient suspected of acute myocarditis.A 75-year-old woman presented with recurrent ventricular tachycardia (VT) compatible with torsades de pointes (TdP) based on sinus bradycardia and QT prolongation. Previously she had received pirmenol, at a serum concentration within therapeutic range, for her paroxysmal atrial fibrillation. Emergent cardiac catheterization identified a ventricular aneurysm of the anteroapical and inferior wall along with angiographically normal coronary arteries. A right ventricular endomyocardial biopsy revealed postmyocarditic change. The left ventricular contraction improved after 5 weeks of conservative treatment. A follow-up echocardiogram revealed transient thickening of partial left ventricular wall consistent with the segment of the aneurysm. Several months later, almost all abnormal findings had improved except for sustained deep negative T waves in precordial leads. Acute myocarditis was primarily suspected as the cause of her clinical presentation.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
6/42. Block of the lower interatrial connections: insight into the sources of electrocardiographic diversities in common type atrial flutter.Whether the conduction disturbances of the interatrial connections play a role in the genesis of ECG variants of atrial flutter is almost completely unknown. We present a patient with typical counterclockwise atrial flutter in whom the ablation of the coronary sinus (CS) area during ongoing atrial flutter produced significant ECG changes without alterations in the activation sequence within the right atrium (RA). This case highlights the possible role of alterations of the interatrial connections in the genesis of atypical ECG manifestations of common type atrial flutter.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
7/42. Fatal arrhythmia in a juvenile athlete due to myocardial hypertrophy and infarction.This report is a case history of a 16-year-old highly trained athlete who suffered from ventricular fibrillation during exhaustive physical activity. After resuscitation and admission into hospital ECG revealed posterior wall infarction. thrombolytic therapy was advised and ST-segment elevation reversed. Within 48 h cerebral edema evolved due to hypoxic brain damage and the subject deceased after 16 days despite prolonged maximum antiedematous therapy. autopsy confirmed the diagnosis of concentric myocardial hypertrophy (total heart weight 568 g) without signs of coronary artery disease. Systemic inflammatory diseases and drug abuse were ruled out by lab studies, evidence for viral infection was not found. Thus, relative coronary insufficiency in regard to myocardial hypertrophy during excessive athletic activity must be viewed as cause for the fatal arrhythmia.- - - - - - - - - - ranking = 2keywords = coronary (Clic here for more details about this article) |
8/42. Cardiogenic shock triggered by verapamil and atenolol: a case report of therapeutic experience with intravenous calcium.Cardiogenic shock developed in a 72-year-old Japanese woman during combination therapy with verapamil and atenolol for recurrent supraventricular arrhythmia. She had coronary atherosclerosis, liver cirrhosis and bradycardia-tachycardia syndrome. Despite of the high-dose catecholamines and counterpulsation, she progressively deteriorated. Bolus administration of intravenous calcium chloride (CaCl2) immediately resolved her hemodynamic collapse.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
9/42. Anteroapical stunning and left ventricular outflow tract obstruction.Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.- - - - - - - - - - ranking = 1keywords = coronary (Clic here for more details about this article) |
10/42. Electrocardiographic ST segment depression.Traditionally, ST segment depression has been associated with acute coronary syndromes; this electrocardiographic pattern may also be found in patients with nonischemic events, such as left bundle branch block (LBBB), left ventricular hypertrophy (LVH), and those with therapeutic digitalis levels. Using the ECG as an adjunct in distinguishing those patients with acute coronary syndromes from those with more "benign," nonacute causes of STSD will obviously lead to divergent treatment and management plans. The following cases illustrate the use the ECG in patients presenting with chest pain and electrocardiographic ST segment depression attributable to an ACS, LVH, LBBB, or digitalis.- - - - - - - - - - ranking = 2keywords = coronary (Clic here for more details about this article) |
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