1/89. 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 = hypertrophy (Clic here for more details about this article) |
2/89. torsades de pointes in a case of hypertrophic cardiomyopathy with special reference to the pathologic findings of the heart including the conduction system.A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.- - - - - - - - - - ranking = 0.2keywords = hypertrophy (Clic here for more details about this article) |
3/89. A probable relationship between an endogenous digitalis-like substance and concentric cardiac hypertrophy in primary aldosteronism.A 44-year-old woman was admitted to our hospital due to severe hypertension. An electrocardiogram (ECG) and an echocardiogram showed severe left ventricular hypertrophy. Her plasma aldosterone level was elevated. magnetic resonance imaging revealed a small mass in the right adrenal gland. Before removal of the tumor, plasma endogenous digitalis-like substance (EDLS) levels were elevated. After removal of the tumor, EDLS levels quickly returned to the normal level. A series of echocardiograms and ECGs over a 6- year period after removal of the tumor showed marked regression of cardiac hypertrophy. These findings suggest that EDLS may be closely related to the development of concentric cardiac hypertrophy in primary aldosteronism.- - - - - - - - - - ranking = 1.4keywords = hypertrophy (Clic here for more details about this article) |
4/89. 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 = hypertrophy (Clic here for more details about this article) |
5/89. Pathological and neuropathological findings in two males with fragile-X syndrome.The present paper addresses post mortem pathological and neuropathological findings in two males with fragile-X syndrome, aged 67 and 87 years. Both subjects died from sudden, unexpected cardiovascular causes, and both showed abnormalities of the mitral valve, ventricular hypertrophy and cardiomegaly. Both cases demonstrated macrocephaly characteristic of the classical Martin-Bell phenotype in FRAXA. There was increased brain weight in both cases: macroscopically, both cerebral and cerebellar hemispheres appeared normal, but dilated lateral ventricles were seen; and microscopic examination of the brain in case 2 showed normal hexalaminar architecture and no gross neuronal dropout. The hippocampus showed mild CA4 pyramidal cell loss and associated gliosis. The cerebellum showed focal Purkinje cell loss and corresponding Bergmann gliosis. Whilst there is a need to delineate the microscopic features of fragile-X syndrome from those of the ageing process, there is an urgent need for more systematic neuropathological studies of fragile-X syndrome; the increased brain weight and Purkinje cell loss in autism and fragile-X syndrome reopens the debate on these two conditions. The case for further research into the cardiac anomalies in fragile-X syndrome is also strengthened by the findings. Finally, the present report confirms the role of interstitial cell hyperplasia as the major cause of megalo-testes in this condition.- - - - - - - - - - ranking = 0.2keywords = hypertrophy (Clic here for more details about this article) |
6/89. Case 3: A patient with systemic hypertension and left ventricular hypertrophy.hypertension is often referred to as the "silent killer" because most hypertensive patients are asymptomatic until cardiovascular sequelae such as stroke, myocardial infarction, heart failure, or renal failure occur. LVH is a common finding in patients with hypertension, especially African-Americans. Data from the Framingham Heart Study indicate that LVH is an independent risk factor for major cardiovascular events. In the amlodipine Cardiovascular Community Trial, 37% of 124 hypertensive patients screened by means of echocardiography had LVH at baseline. Although there was no difference in the prevalence of LVH by gender or age, African-American patients were nearly twice as likely to have LVH than white patients (64% vs. 34%, p<0.05). Hence, aggressive therapy to reach target goals outlined in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High blood pressure (JNC VI) is especially important in this group of patients. Even lifestyle modifications such as weight reduction and limitation of salt intake, if sufficiently aggressive, can lead to regression of LVH, as demonstrated by results of the Treatment of Mild hypertension Study (TOMHS). Most classes of antihypertensive drugs are effective in causing regression of LVH. Vasodilators, such as minoxidil and hydralazine, do not have an effect on regression, possibly because reflex tachycardia and stimulation of catecholamines and the renin-angiotensin system associated with these agents may negate the benefit of reduced afterload. There is some controversy regarding the ability of the angiotensin receptor blockers to reduce LVH. In some studies, these agents were associated with regression, whereas in others they were not. Whether targeting LVH as the primary treatment goal in hypertensive patients will have long-term benefits on outcome above and beyond simply reducing blood pressure is not clear.- - - - - - - - - - ranking = 0.8keywords = hypertrophy (Clic here for more details about this article) |
7/89. 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 = 0.8keywords = hypertrophy (Clic here for more details about this article) |
8/89. Transient right sided hypertrophic cardiomyopathy in an infant born to a diabetic mother.Hypertrophic cardiomyopathy (HCM) is a rare primary myocardial disease, characterized by hypertrophy of the left and/or right ventricle. Infants of diabetic mothers (IDM) are at risk for development of HCM, respiratory distress and persistent pulmonary hypertension. A case of severe right sided HCM in an infant born to a diabetic mother is presented. The patient's findings were complementary to the previous observations reporting HCM in IDM. The presence of disproportionate septal hypertrophy in the echocardiography of an infant born to a diabetic mother is highly suggestive of HCM in IDM. In our opinion, further cardiac evaluation is not indicated unless other cardiac abnormalities are suspected.- - - - - - - - - - ranking = 0.4keywords = hypertrophy (Clic here for more details about this article) |
9/89. Long-term results of apico-aortic valved conduit for severe idiopathic hypertrophic subaortic stenosis.We report our long-term results of apico-aortic conduit implantation in patients with isolated idiopathic hypertrophic subaortic stenosis. Between December 1977 and July 1983, apico-aortic prosthetic-valved conduits were implanted in 4 such patients (age range, 24-65 years) who had severe left ventricular hypertrophy and small left ventricular chambers. In this procedure, the distal end of the conduit was anastomosed to the ascending aorta in 3 patients and to the upper abdominal aorta in 1. Postoperative echocardiography showed relief of the left ventricle-aortic gradient and enlargement of the left ventricular chamber in all cases. One patient died of perioperative wound infection. One patient died of unnatural causes 13 years after the initial operation; in his case, the conduit was known to be occluded. Two patients are alive 15 and 19 years, respectively, after the initial operation. Three instances of conduit obstruction due to bioprosthetic calcification were observed. Despite the high incidence of reoperation due to conduit valve failure, apicoaortic conduit implantation has produced good hemodynamic outcome and has improved the quality of life in patients who have idiopathic hypertrophic subaortic stenosis and anatomic features unsuitable for Morrow's operation. Improvements in bioprostheses and in apical implantation techniques may allow a revival of apico-aortic conduit implantation in selected patients with idiopathic hypertrophic subaortic stenosis.- - - - - - - - - - ranking = 0.2keywords = hypertrophy (Clic here for more details about this article) |
10/89. Antihypertensive therapy reduces increased plasma levels of adrenomedullin and brain natriuretic peptide concomitant with regression of left ventricular hypertrophy in a patient with malignant hypertension.We investigated the potential role of increased plasma adrenomedullin and brain natriuretic peptide (BNP) levels in a patient with malignant hypertension. A 51-year-old man was admitted to our hospital with a chief complaint of visual disturbance. His blood pressure was 270/160 mmHg on admission. Papillary edema associated with retinal bleeding was observed. echocardiography revealed marked concentric left ventricular hypertrophy with mild systolic dysfunction. plasma levels of adrenomedullin and BNP were markedly elevated. Antihypertensive therapy reduced the plasma levels of adrenomedullin in association with a concomitant decrease in blood pressure. The plasma level of BNP also decreased and regression of left ventricular hypertrophy and normalization of left ventricular systolic function were observed. Our findings suggest that adrenomedullin may be involved in the defense mechanism against further elevations in blood pressure in patients with hypertension and that the plasma level of BNP may reflect left ventricular systolic dysfunction, left ventricular hypertrophy, or both, in patients with severe hypertension.- - - - - - - - - - ranking = 1.4keywords = hypertrophy (Clic here for more details about this article) |
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