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

To investigate the predisposing factors and the clinical significance of the musical aortic component of the second heart sound (musical S2), 18 patients with musical S2 (musical group) among the consecutive 2,000 patients with phonocardiographic examination were noninvasively studied by analyzing underlying diseases, phonocardiographic findings, organic changes of the aortic valve, severity of aortic regurgitation and left ventricular dysfunction. Organic changes of the aortic valve were assessed by two-dimensional echocardiography, and aortic regurgitation was assessed by color Doppler flow imaging. Twenty-two normal subjects (normal group) and 17 patients with essential hypertension (hypertensive group) served as controls. Mean ages were matched among the three groups. 1. Left ventricular dilatation (seven patients) and hypertension (six patients) were the dominant part of underlying disease in the musical group. 2. Musical S2 was classified in the following two types based on the phonocardiographic characteristics; musical vibrations followed immediately after the accentuated S2, and the S2 which was replaced by regular vibratory waves. 3. Frequency of the musical vibrations ranged from 120 to 200 Hz, and its duration ranged from 60 to 120 msec. Amplitude of the musical vibrations decreased by inhalation of amyl nitrite, but increased by infusion of methoxamine. In a case with mild rheumatic valve disease, methoxamine induced marked intensification of the amplitude and prolongation of the duration of the musical vibrations, finally giving a typical cooing murmur. 4. Echo intensity of the aortic valve tended to be higher in the musical group than in the other two groups. 5. Echocardiographically, aortic regurgitation appeared more frequently in the musical group (88%) than in the normal (36%) and hypertensive (41%) groups. Area of the aortic regurgitant signal was significantly larger in the musical group (4.1 +/- 1.4 cm2) than in the normal (1.2 +/- 0.8 cm2) and hypertensive (2.3 +/- 1.2 cm2) groups. 6. Left ventricular end-diastolic dimension was significantly larger in the musical group (5.8 +/- 0.6 cm) than in the normal (4.7 +/- 0.5 cm) and hypertensive (4.8 +/- 0.7 cm) groups. Fractional shortening of the left ventricle was significantly smaller in the musical group (26 +/- 10%) than in the normal (37 +/- 5%) and hypertensive (37 +/- 8%) groups. In a case of the musical group, musical vibrations following the S2, which was large in amplitude at the state of heart failure, decreased markedly after the recovery from heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Possible mechanism of production of the musical second heart sound and its clinical significance]. 188 56

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. 213 51

This study correlates variables derived from blood pressure (BP) and heart rate (HR) monitoring with the degree of left ventricular structural changes in essential hypertension. Forty patients with mild-to-moderate hypertension according to World Health Organization criteria underwent 24-hour ambulatory monitoring. Echocardiographic (posterior wall and interventricular septum thickness, left ventricular mass) or ECG (SV1 + RV5) indices of hypertrophy were significantly (p less than 0.01) correlated (positive correlations) with derivatives of BP monitoring (mean systolic and diastolic BP values) but not with HR derivatives. Echocardiographic indices of dilatation (left ventricular end-diastolic volume and diameter) were significantly (p less than 0.01 to less than 0.001) correlated (negative correlations) with derivatives of HR monitoring (mean HR values, mainly during the night) but not with BP derivatives. It is concluded that in essential hypertension, left ventricular hypertrophy depends on mean 24-hour systolic and diastolic BP values, whereas left ventricular dilatation appears to be more prominent in patients with bradycardia mainly during the night.
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PMID:Effect of 24-hour blood pressure and heart rate variations on left ventricular hypertrophy and dilatation in essential hypertension. 213 39

Abnormalities in the diastolic function of the left ventricular pump are the common determinant and, above all, the earliest manifestation of all forms of chronic left ventricular failure, whether or not the left ventricular systolic function is abnormal. Congestive signs, in particular, are directly related to abnormalities of ventricular filling. Primary diastolic dysfunction is the cause of left ventricular failure in about 40 p. 100 of the cases, but it may also be observed in almost all cardiopathies. In myocardial ischaemia the pressure-volume relation is displaced upwards owing to a slowed down, inhomogeneous and incomplete relaxation. Left ventricular hypertrophy, whether it is due to excessive pressure (arterial hypertension, aortic stenosis) or reflects a primary hypertrophic cardiomyopathy, is associated with a slowing down of ventricular relaxation and a reduction of left ventricular diastolic distensibility, even though the ventricular pump systolic function remains normal for a long time. Outside alterations in the distensibility of the ventricular muscle, ventricular dilatation alters ventricular filling by forcing the ventricle to function on the vertical part of its diastolic pressure-volume relation. Nowadays, the aged hearts is the most frequent cause of heart failure with normal systolic function. In all cases dysrhythmias and atrioventricular desynchronization act as aggravating factors. Treatment is often difficult since positively inotropic drugs or arterial vasodilators frequently have a modest or even deleterious effect.
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PMID:[Disorders of diastolic function in chronic left ventricular insufficiency]. 214 34

Twenty cases of ependymomas of the intradural filum terminale in adults have been reviewed. Their pathology was quite uniform, of a myxopapillary type, similar to the low grade ependymoma described by Kernohan, which represent about 23% of the tumours of cauda equina. Mean age of the patients was 35.7 years. Mean time between the first symptom and the diagnosis was 46 months. Clinical symptoms were often non specific, with low back pain and radiculalgias. At the time of operation, clinical signs were essentially motor deficits usually moderate (11 cases), sphincter disturbances (10 cases), and sensory loss (9 cases). In 3 patients with rapid worsening, an intratumoral haemorrhage was found. In 2 other cases, intracranial hypertension was the main symptom: in the first, it was related to hydrocephalus probably caused by spinal subarachnoid haemorrhage; in the second, there was no ventricular dilatation. In this series, neuroradiological examinations had consisted mainly in myelographies. C.T. scan has been performed in 3 patients; in only one case it has allowed to visualize a presacral extension. One patient had preoperative M.R.I.: the association of an expansive lesion with upper cyst in conus medullaris and presence of blood in the sacral area permitted the diagnosis of ependymoma of the filum terminalis. The average size of the tumours was 8 cm. Total removal has been possible in 15 cases (and in 2 of the 5 giant tumours), subtotal removal in 2 cases, and partial removal in 3 cases. In 4 patients where existed an intraspinal cord extension above the conus, it has been resected completely, except for one case with recurrence. Patients with a total removal had a good functional recovery (13/15). No recurrence has been observed in this group. In conclusion, with M.R.I., one may hope an earlier diagnosis, condition of radical surgery. So, radiotherapy which is not without risk, could be avoided.
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PMID:[Ependymoma of the intradural filum terminale in adults. 20 cases]. 216 65

Hydrocephalus with spinal tumor is rare, and its cause is obscure. We report one patient with a thoracic astrocytoma who developed ventricular dilatation and intracranial hypertension. The pathophysiology is reviewed.
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PMID:Hydrocephalus and intraspinal tumor in childhood. 234 May 27

Doppler echocardiography has become a very useful and widely employed imaging technique for evaluating valvular regurgitation, and has thus lead to the discovery of regurgitation in unexpected subjects. In this study, we examined left-sided valvular regurgitation in 31 healthy subjects, 35 patients with hypertension and 43 patients with old myocardial infarction by Doppler echocardiography. Aortic regurgitation was found in 3% of healthy subjects, 8% of hypertensive patients and 5% of patients with myocardial infarction. Mitral regurgitation was found in 35% of healthy subjects, 69% of hypertensive patients and 84% of patients with myocardial infarction. The pathogenesis of mitral regurgitation in hypertension is considered to be the impairment of the mitral leaflets, since neither anatomical nor functional abnormalities were found in the subvalvular mitral apparatus. Left ventricular dilatation and asynergy near the papillary muscles were related to the pathogenesis of mitral regurgitation in myocardial infarction. Mitral regurgitation in healthy subjects and hypertensive patients was mild and resistant to afterload stress, suggesting that it was less pathological. On the other hand, mitral regurgitation in myocardial infarction was easily worsened by afterload stress. Doppler echocardiography has thus provided us with new insights into valvular regurgitation in healthy subjects and patients without rheumatic valvular disease.
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PMID:Evaluation of left-sided valvular regurgitation in healthy, hypertensive and myocardial infarction subjects by Doppler echocardiography. 236 14

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

65 patients with negative but technically satisfactory 4 vessel angiography - all admitted to our Department in the years 1976-1983 - were evaluated in the present study. CT scan was undertaken in all cases (in 47 cases within 4 days of haemorrhage). Arterial hypertension was present on admission in 9% of cases. The period of follow-up ranged from 4 to 11 years, with a mean of 5.3 years. The study group was compared to a control group, comprising 760 patients with subarachnoid haemorrhage from ruptured aneurysms, admitted during the same period. Clinical grade on admission (Hunt's classification) was better in patients belonging to the study group. The amount of cisternal deposition on CT scan was less significant than in patients with ruptured aneurysms, and the deposition was often atypical (circumpeduncular, ambiental, and/or tentorial). Clinical deterioration associated with vasospasm was observed in 5% of patients in this study and in 27% of patients in the control group. In patients with a consistent or thick cisternal layer (CT scan "at risk") the incidence of clinical vasospasm was 21%, against 47% in controls. One or more rebleedings occurred in 12% of patients in the study group, against 25% of patients in the control group. A significant ventricular dilatation was observed in 15% of patients in the first group (requiring a shunt in 8%), against 25% of patients in the second group (requiring a shunt in 11%). Final outcome was favourable in 95% of patients in this study group and in 63% of patients in the control group, with a mortality rate of 5% in the first group and 32% in the second group.
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PMID:Subarachnoid haemorrhage of unknown origin: clinical and tomographical aspects. 271 94

Echocardiography was performed for 246 patients with hypertension. Among the 246 patients, echocardiographic features simulating dilated cardiomyopathy (DCM) were observed in 12. These patients had past history of hypertension and prominent left ventricular dilatation with reduced left ventricular contractility, but no left ventricular wall thickening. To elucidate the mechanism producing DCM-like features in patients with hypertension, the clinical and echocardiographic findings of the 12 hypertensive patients (HT-DCM) were compared with those of 50 hypertensive patients without dilated left ventricles and of 31 patients with DCM. On admission, all patients with HT-DCM had congestive heart failure (CHF) without high blood pressure and their echocardiograms revealed the abnormal findings described above. There were no differences of the clinical and echocardiographic findings on admission between HT-DCM and DCM. Following medical treatment, relatively early improvement of CHF was noted in all patients with HT-DCM; the LV dimension decreased and diffuse wall motion abnormality improved steadily with gradual elevation of blood pressure during the follow-up periods. The LV function of most patients with HT-DCM improved markedly but never reached normal levels. There were no significant differences the right ventricular endomyocardial biopsy findings of between DCM and HT-DCM. It was suggested the DCM-like features in these cases are caused, not only by hypertension, but by other factors, as well.
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PMID:[Hypertensive heart disease simulating dilated cardiomyopathy]. 294 71


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