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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of fibrosis was studied quantitatively in the entire left ventricular wall of a transverse slice of the heart from 10 necropsy cases of hypertrophic cardiomyopathy, 10 cases of hypertensive heart disease, and 20 normal adults. The percentage area (mean (SD)) of fibrosis in the left ventricular wall in hypertrophic cardiomyopathy (10.5 (4.3)%) was significantly greater than that in hypertensive heart disease (2.6 (1.5)%) or in normal hearts (1.1 (0.5)%). In hypertrophic cardiomyopathy the percentage area of fibrosis was greater (13.1 (4.8)%) in the ventricular septum than in the left ventricular free wall (7.7 (4.2)%) whereas in hypertensive heart disease and normal hearts values in these two areas were similar. The percentage area of fibrosis in the left ventricular free wall (where myocardial fibre disarray was not extensive even in hypertrophic cardiomyopathy) was greater in hypertrophic cardiomyopathy than in hypertensive heart disease. The percentage area of fibrosis correlated with heart weight in hypertensive heart disease, but not in hypertrophic cardiomyopathy. These results suggest that widespread fibrosis in hypertrophic cardiomyopathy cannot be explained by cardiac hypertrophy alone, and that disarray and other factors are also important in pathogenesis. The increase in the percentage area of fibrosis from the outer to the inner third of the left ventricular free wall in hypertrophic cardiomyopathy and in hypertension probably reflected transmural gradients of wall stress and myocardial fibre diameter. Although fibrosis is not specific to hypertrophic cardiomyopathy, its quantification and analysis of its regional distribution provide information that is useful in investigating the pathophysiology of the disorder.
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PMID:Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy. 371 96

This is a report of a patient with mitral valve prolapse (MVP) and myocardial abnormalities on endomyocardial biopsy in whose relatives hypertrophic cardiomyopathy (HCM) was identified. A 19-year-old woman was admitted to our hospital for evaluation of a heart murmur. A systolic ejection murmur was audible in the third intercostal space at the left sternal border, and a standard 12-lead electrocardiogram showed ST-T wave changes in leads II, III and aVF. Echocardiography revealed prolapse of the anterior leaflet of the mitral valve, but no left ventricular hypertrophy. Endomyocardial biopsy disclosed mild hypertrophy and disarrangement of the myocardium. The family study revealed asymmetrical septal hypertrophy in her mother, who had no history of hypertension. Her younger sister had mild hypertrophy of the interventricular septum on echocardiography, and her histopathological findings suggested a diagnosis of HCM. This case was clinically regarded as MVP, but development of left ventricular hypertrophy as noted in her mother may occur in the future.
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PMID:[Mitral valve prolapse with myocardial disarrangement and familial hypertrophic cardiomyopathy: a case report]. 378 85

To investigate whether bizarre myocardial hypertrophy with disorganization (BMHD) is characteristic of hypertrophic cardiomyopathy (HCM), the histopathology of the biopsied left ventricular myocardium in 18 patients with essential hypertension (HT) and 14 patients with HCM was studied. A "biopsy score" was devised for a more quantitative evaluation of the BMHD and a comparative study on the biopsy score of the left ventricular biopsied specimen was also performed. The patients with HT were judged to be in stages I or II of the WHO criteria and had a history of hypertension of more than 5 years. The BMHD was defined as myocardial cells showing hypertrophy, disorganization, and bizarre nuclei. "Disorganization" of myocardial cells was distinguished both by the terminology and histopathological characteristics from "disarrangement" of myocardial cells. The biopsy score employed four factors and was determined according to the following formula: Biopsy score = hypertrophy of myocardial cells + (disorganization of myocardial cells) x 2 + bizarre nuclei + whorling of muscle bundles. Both the hypertrophy and the disorganization of myocardial cells were regarded as essential conditions indicating the presence of BMHD. The BMHD was found in 2 of 18 patients with HT (11%) and in 10 of 14 patients with HCM (71%) in the left ventricular biopsied specimens (P less than 0.005). However, "disarrangement" of myocardial cells was found in 13 of 18 HT patients (72%) and in 10 of 14 HCM patients (71%) in the left ventricular biopsied specimens, showing no difference between the two groups. The biopsy score in HCM patients was larger than that found in HT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular endomyocardial biopsy findings in patients with essential hypertension and hypertrophic cardiomyopathy with special reference to the incidence of bizarre myocardial hypertrophy with disorganization and biopsy score. 383 Oct 23

To evaluate differences in systolic global and regional performances of the left ventricle during exercise, multi-stage submaximal exercise echocardiography was used for 21 patients with hypertrophic cardiomyopathy (HCM) and 14 patients with systemic hypertension (HT), whose interventricular septa (IVS) were nearly the same in thickness (HCM; 16.5 +/- 2.4 mm, HT; 15.4 +/- 1.7 mm, NS). The data were compared with those of 18 normal subjects (N). During exercise, end-diastolic dimension (EDD) was increased in all three groups; however, there was no statistical differences among the three groups either at rest or during exercise. End-systolic dimension (ESD) was significantly decreased during exercise in HT (29.3 +/- 5.8 at rest to 28.1 +/- 5.8 mm at the peak exercise, p less than 0.05) and N (from 30.3 +/- 3.3 to 25.7 +/- 3.0 mm, p less than 0.001). On the other hand, ESD of HCM at rest, which was less than those of the other two groups, did not decrease with exercise (from 25.1 +/- 4.5 to 25.6 +/- 4.6 mm, NS), and rather they increased (more than 2 mm) during exercise in seven patients. The % shortening fraction (%SF) increased from rest to exercise both in HT (35.6 +/- 7.9% to 40.1 +/- 9.6%, p less than 0.001) and in N (from 35.1 +/- 4.2 to 45.9 +/- 4.7%, p less than 0.001). However, in the HCM group, the %SF, which was significantly greater at rest than in the other two groups, did not increase during exercise (42.5 +/- 6.8 to 42.5 +/- 8.8%, NS). In addition, in seven of 21 patients with HCM, the %SF increased more than 5% at the peak exercise. At rest, systolic wall thickening (%WT) of the IVS equally reduced both in HCM and HT. It increased in HT from 20.8 +/- 9.3% at rest to 24.6 +/- 12.7% at the peak exercise (p less than 0.05), but did not change in HCM (from 16.6 +/- 9.6% to 16.3 +/- 7.0%, NS). At rest, %WT of the left ventricular posterior wall (LVPW) was significantly greater in HCM than in HT. During exercise, it increased in HT (from 43.1 +/- 15.9% to 61.9 +/- 20.5%, p less than 0.01), but did not increase in HCM (from 81.0 +/- 27.7% to 85.5 +/- 29.6%, NS).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differences in left ventricular systolic performance during exercise in patients with hypertrophic cardiomyopathy and systemic hypertension]. 384 86

The accuracy of a newly developed nuclear magnetic resonance-computed tomography (NMR-CT) technique in diagnosing idiopathic cardiomyopathy was assessed and compared with other procedures such as echocardiography, coronary angiography, left ventriculography, myocardial biopsy, and electrocardiography. In case 1, the NMR-CT clearly revealed thickening of the lateral ventricular free wall and ventricular septum, which strongly suggested hypertrophic cardiomyopathy. Catheterization showed a pressure gradient of 54 mm Hg and this patient was diagnosed as having hypertrophic obstructive cardiomyopathy. In case 2, the NMR-CT showed dilatation of the ventricular cavity indicative of dilated cardiomyopathy. This was confirmed by echocardiography, which revealed the enlarged cavity of the ventricle and poor movement. In case 3, the patient had marked hypertension; the cardiac silhouette was enlarged, but the NMR-CT revealed that the ventricular free wall and septum were of normal thickness. This study shows that NMR-CT is of value in the differential diagnosis of idiopathic cardiomyopathy.
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PMID:Clinical application of NMR-CT for idiopathic cardiomyopathy. 391 78

The circumstances surrounding 60 sudden deaths (59 men, one woman) associated with squash playing are described. The mean age (SD) of those who died was 46 (10.3) years (range 22-66 years). Necropsy reports were available in 51. The certified cause of death was coronary artery disease in 51 cases, valvar heart disease in four, cardiac arrhythmia in two cases, and hypertrophic cardiomyopathy in one case. There were only two deaths from non-cardiac causes. Forty five of those who died had reported prodromal symptoms, the most common of which was chest pain, and 22 were known to have had at least one medical condition related to the cardiovascular system during life, the most common of which was systemic hypertension (14 subjects). Those dying from coronary artery disease had a high frequency of risk factors. Some of these deaths might have been prevented by appropriate counselling of players after prospective medical screening, which would have detected most of the patients with overt cardiovascular disease and some of those with subclinical coronary artery disease.
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PMID:Sudden death and vigorous exercise--a study of 60 deaths associated with squash. 394 53

Left ventricular hypertrophy is caused by a wide variety of cardiovascular conditions, including systemic hypertension, aortic valvular disease, and hypertrophic cardiomyopathy. This paper describes a case of diffuse hypoplasia of the aorta in left ventricular hypertrophy. This condition has not previously been well documented. We emphasize the need for evaluation of aortic dimension when systolic hypertension and vascular bruits are observed in association with myocardial hypertrophy.
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PMID:Diffuse hypoplasia of the aorta as a possible cause of cardiac hypertrophy. 403 97

To delineate the precise anatomic abnormalities of the interventricular septum (IVS), mitral valve (MV), and left ventricular posterior wall (LVPW) in patients with hypertrophic cardiomyopathy (HCM), we used axial biventriculography (BVG) (hepato-clavicular projection: angled BVG) to examine 17 patients with HCM and four with concentric hypertrophy due to systemic hypertension. We also examined 9 of these 21 patients with conventional left anterior oblique (LAO) BVG (non-angled BVG). The IVS and along axis of the LV cavity when measured by angled BVG were significantly longer than when measured by non-angled BVG. The IVS, MV, and LVPW were better seen in profile in angled than in non-angled BVG. In two patients with HCM with obstruction (HOCM), systolic anterior motion of the anterior leaflet of the MV was readily identifiable with angled BVG, which is usually not the case with non-angled BVG. Thus, angled BVG is superior to conventional LAO BVG in the angiographic assessment of patients with HCM.
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PMID:Improved evaluation of hypertrophic cardiomyopathy by biventriculography with axial projection. 404 Mar 19

Whether giant negative T waves (GNT) of 1 mV or greater represent the electrocardiographic characteristics of idiopathic cardiomyopathy, particularly apical hypertrophic cardiomyopathy, is controversial. To clarify this point, a comparative study was conducted for 57 persons with GNT (GNT+ group) and 57 persons of hypertrophic cardiomyopathy with either asymmetric septal hypertrophy or diffuse hypertrophy of the ventricular wall in the absence of GNT (GNT- group). Patients with cerebral vascular accidents, myocardial infarctions, valvular heart disease, myopericarditis, and implanted pacemakers were excluded from the study because these patients' ECGs may show GNT. Left ventriculograms were investigated at end-diastole in the right anterior oblique projection. The GNT+ group showed a spade-like configuration indicating a marked reduction in the lumen of the apical cavity in 25 cases (43.9%); a kidney or banana-like configuration indicating the inferior wall bulging into the left ventricular cavity in its mid-zone in eight cases (14.0%), and an oval configuration which indicated no deformity of the left ventricular cavity in 24 (42.1%). The spade-like configuration was also seen in four cases (7.0%) of the GNT- group. A study of ventricular wall thicknesses based on left ventriculography showed that 25.5% of cases with GNT did not have concomitant apical hypertrophy. Generally, the GNT+ group cases had a significantly thicker anterior left ventricular wall and apical hypertrophy compared to the GNT- group. The hypertrophic states of the apical wall and anterior wall of the left ventricle correlated well. The GNT+ group included a significantly larger percentage of patients who were middle aged and older than did the GNT- group, and the frequency of accompanying hypertension was significantly higher in the former. The confirmed or suspected familial occurrence of cardiomyopathy (CM) was observed in 32 cases (56.1%) of the GNT- group, and in 18 cases (31.6%) of the GNT+ group, i.e., the incidence was significantly lower in the GNT+ group. In an endomyocardial biopsy study, 40 cases (70.1%) of HCM without GNT had bizarre myocardial hypertrophy with disorganization (BMHD). The incidence of BMHD in the GNT+ group was 21/57 (36.8%)-significantly lower than in the GNT- group. In the GNT- group, there was no significant difference in the incidence of BMHD between relatively young and old patients or between patients with and without accompanying hypertension; whereas, in the GNT+ group, it was significantly lower among those with accompanying hypertension and in older patients than in those without accompanying hypertension and in younger patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Do giant negative T waves represent apical hypertrophic cardiomyopathy? Left ventriculographic and cardiac biopsy studies]. 406 55

Although apical hypertrophy is characterized by a spade-like configuration of the left ventricle and giant negative T waves on electrocardiograms, the identity of apical hypertrophy in the disease spectrum of hypertrophic cardiomyopathy (HCM) is not fully established. The present study compared the demography, familial occurrence, and acquired factors of 43 patients who had apical hypertrophy with those of 104 patients who had asymmetric septal hypertrophy (ASH). Demographically, apical hypertrophy occurred predominantly in middle-aged males (86%). Family surveys showed that 13% of siblings of apical hypertrophy were affected, significantly less than in obstructive (31%) or non-obstructive (29%) HCM with ASH. Thirty-eight percent of siblings of ASH patients less than 35 years of age were affected, with a male/female ratio of 4/5, suggesting an autosomal dominant inheritance. The acquired factors associated with apical hypertrophy were assessed in a case-control study. Relative risk (odds ratio) of the condition was 3.46 (p less than 0.05) in those with histories of hypertension, and increased further to 8.09 (p less than 0.001) in those who were often hypertensive according to their physician's evaluations. Thus a strong association of hypertension with apical hypertrophy was suggested. However, hypertension in this condition was usually mild and labile, the blood pressure reverted to the normal range within several days of hospital admission, implying that transient hypertension during daily activity is associated with apical hypertrophy. Therefore, blood pressure response during exercise stress tests of 25 patients with apical hypertrophy was compared with that of age- and sex-matched controls. Slopes of linear regression between systolic blood pressure and heart rate and oxygen consumption during exercise, were used as indices of blood pressure response. They were significantly greater in apical hypertrophy than in the controls (1.2 +/- 0.4 vs 0.9 +/- 0.3, p less than 0.01 and 4.3 +/- 1.7 vs 2.8 +/- 0.8, p less than 0.001). This trend was observed even in patients without histories of hypertension. These findings suggested that apical hypertrophy has an inheritance pattern different from that of ASH, and has a possible association with acquired factors such as hypertension. Therefore, apical hypertrophy seemed to be a disease entity distinct from HCM with ASH, though it might be included in the disease spectrum of HCM.
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PMID:[Apical hypertrophy and its genetic and acquired factors]. 406 57


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