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

1. The myocardial collagen matrix is an active participant in determining ventricular architecture and diastolic function, and myocardial structural integrity and mechanical properties. It consists of a network of fibrillar collagen which is intimately related with the myocyte, myofibril and muscle fiber as well as the coronary vasculature. Consisting primarily of collagen types I and III, this material exhibits a high tensile strength which, even though normally present in relatively small amounts, plays an important role in the behavior of the ventricle during diastole. 2. Removal of less than half of the normal amount of collagen results in a dilated ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricular histologic and functional alterations are evident during ischemia and in dilated cardiomyopathy. Thus, it would appear that a chronic change in the shape and size of the heart must be preceded by alterations in the interstitial collagen matrix. 3. With elevations in the circulating levels of angiotensin and/or mineralocorticoids, the hypertrophic response of the myocardium to the accompanying hypertension includes a progressive remodeling of the collagen component. Typically there is an increase in collagen concentration, thickening of existing fibrillar collagen and the addition of new collagen at all levels of the matrix. The consequences of this remodeling are an adverse alteration of the passive mechanical properties of the myocardium and LV diastolic dysfunction. This pathophysiologic aspect of the hypertrophic process is independent of the concomitant remodeling of the myocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial collagen remodeling and left ventricular diastolic function. 134 31

Cardiac involvement in 75 cases (mean age 21.1 +/- 6 years) with non-specific aorto-arteritis was studied. Detailed clinical examination, echocardiography and cardiac catheterization, including angiography, were done in all the cases, as was coronary angiography. Features of cardiac failure like sinus tachycardia, cardiomegaly, left ventricular third heart sound gallop and pulmonary congestion were detected in 27 cases with reduction of left ventricular ejection fraction (25-48%). Systemic hypertension was seen in 60 cases. Central aortic pressure, left ventricular systolic pressure and left ventricular end-diastolic pressure were increased in 66 cases. Pulmonary hypertension and increased pulmonary vascular resistance were detected in 6 cases. Aortic and mitral regurgitation were seen in 15 and 12 cases, respectively. Three patients had features of dilated cardiomyopathy such as generalized cardiomegaly, systemic and pulmonary congestion but without any cardiac murmurs and with normal central aortic pressure. The coronary angiogram revealed obstruction of the left anterior descending artery in 3 cases and right coronary artery obstruction in another 3 cases. Histopathological studies revealed non-specific inflammatory changes with fibrosis in cardiac musculature and the great vessels.
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PMID:Cardiac involvement in non-specific aorto-arteritis. 134 27

Congestive heart failure (CHF) is a common manifestation of hypertension, coronary artery disease, and dilated cardiomyopathy. The Framingham study showed that the incidence of CHF increases twofold with each decade of age. The presence of CHF increases the age-adjusted death rate 5.5-fold for women and 8-fold for men, and it increases the sudden death rate 5.5-fold in both men and women. Ventricular arrhythmias are a common accompaniment of CHF. Ambient ventricular premature complexes occur in most of these patients, and nearly one half of all CHF patients will have nonsustained ventricular tachycardia on a 24-h ambulatory electrocardiographic (Holter) recording. In addition, low left ventricular ejection fraction (LVEF) predicts inducible sustained ventricular tachycardia on electrophysiologic study. One-year mortality increases with worsening New York Heart Association (NYHA) Functional Class and decreasing LVEF. As the overall yearly mortality increases, the proportion of patients who die of arrhythmias decreases. The precise mechanism of death is frequently difficult to assess. Nonarrhythmic causes of death include CHF, shock, electromechanical dissociation, and myocardial rupture. Arrhythmic causes are most commonly due to ventricular tachycardia/ventricular fibrillation. Bradycardic events (asystole or heart block) are usually associated with progressively worsening CHF. Noncardiac causes that may confuse classification include pulmonary embolus and cerebrovascular accident. Because many patients have ischemic heart disease as the etiology of the CHF, a recurrent ischemic event can likewise make classification difficult. Overall, approximately one half of all deaths in CHF are arrhythmic and one half are nonarrhythmic.
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PMID:Clinical significance and management of arrhythmias in the heart failure patient. 139 10

Although slightly affected by alterations in preload, the maximum first derivative of left ventricular pressure with respect to time, Max(dP/dt), is widely regarded as a simple and convenient index of cardiac contractility for clinical use. The feasibility of noninvasive, hence repeatable, measurement of Max(dP/dt) will certainly lead to re-evaluation of its usefulness. Max(dP/dt) is given by the following equation: Max(dP/dt) = rho c Max(du/dt), where rho is the blood density, c the pulse wave velocity, and mu the flow velocity in the aorta. This equation has been previously validated in animal experiments and has now been applied to the clinical setting for the first time. In 20 patients without aortic stenosis, left ventricular pressure was measured with a catheter-tip micromanometer, aortic ejection flow velocity was measured by Doppler echocardiography, and pulse wave velocity by mechanocardiography or Doppler echocardiography. Then, delta c Max (du/dt was calculated from the measured data and compared with measured Max (dP/dt). A significant positive correlation was found between them (rho c Max (du/dt) = 0.96 x Max (dP/dt) + 6.52, r = 0.83, p < 0.001). In 11 patients with hypertension, rho c Max (du/dt) was obtained before and after long-term (average 13.1 months) treatment with antihypertensive drugs. In spite of the expected reduction in blood pressure and the regression of left ventricular mass, rho c Max (du/dt) remaioned unchanged. In 9 patients with dilated cardiomyopathy, the effects of beta 1-agonist were tested at the beginning of therapy (30 mg/day denopamine) and 6 months later. The increase in rho c Max (du/dt) observed 1 hour after oral administration of he drug had not changed significantly 6 months later. We conclude that the index rho c Max (du/dt), is useful in assessing the contractile state of the left ventricle noninvasively.
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PMID:A noninvasive method of measuring Max(dP/dt) of the left ventricle by Doppler echocardiography. 149 80

To determine whether obvious hemodynamic advantages of continuous ambulatory peritoneal dialysis (CAPD) over intermittent hemodialysis are reflected in superior cardiac structure and function, 16 of 55 analyzed CAPD patients (CAPD duration: 28 months) were followed over 35 months with echocardiography in a prospective analysis: 26 patients had died. LV dimensions (end-diastolic: 52 +/- 7 vs. 51 +/- 8 mm; control vs. follow-up) and systolic function (ejection fraction: 63 +/- 10 vs. 59 +/- 14%) were normal. Major findings were an increase in the amount of initially observed LV hypertrophy (251 +/- 68 vs. 342 +/- 135 g; p less than 0.03) and a decrease in mean LV volume/mass ratios (0.73 +/- 0.17 vs. 0.54 +/- 0.13; p less than 0.001). Excluding patients with dilated cardiomyopathy and valve disease, the amount of progression in LV hypertrophy was related directly to mean arterial pressure and cardiac output (n = 12; p less than 0.02) despite extensive use of antihypertensive medication (1.9 +/- 1.3 vs. 1.5 +/- 1.4 drugs/patient). No correlation was found with diastolic blood pressure, hemoglobin, serum parathyroid hormone, creatinine, urea, age, or CAPD duration. We conclude that LV hypertrophy is frequent in CAPD patients and further increases during long-term CAPD treatment. Factors contributing to the progression of LV hypertrophy are hypertension and hypercirculation.
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PMID:Progression of left ventricular hypertrophy in end-stage renal disease treated by continuous ambulatory peritoneal dialysis depends on hypertension and hypercirculation. 153 53

The frequency, clinical characteristics, and outcome of patients admitted with heart failure to a district general hospital in North-West London serving a population of approximately 155,000 was assessed over a six-month period. The number of patients with heart failure was determined by both a prospective ward survey and a retrospective study of all patient records with diagnostic codes for heart failure or pulmonary oedema. During those six months, 2,877 patients were admitted to the medical and geriatric services of whom 140 (4.9%) had heart failure. Only 29 patients in heart failure were under the age of 65 years. In 86 patients the mode of presentation was acute pulmonary oedema. Fifty-two (37%) patients had an arrhythmia at the time of admission of whom 48 had atrial fibrillation. An electrocardiogram, a chest X-ray, and an echocardiogram were performed in 137, 136, and 81 patients respectively. The aetiology of heart failure was considered to be coronary artery disease (41%), valve disease (9%), hypertension (6%), cor pulmonale (4%), a dilated cardiomyopathy (1%), congenital heart disease (1%), thyrotoxicosis (1%), and unknown (36%). During the period of hospital stay 42 patients (30%) died; a further 20 patients (14%) died in a one-year follow-up. In a district general hospital heart failure is a common reason for admission and patients remain in hospital for a considerable time. Arrhythmias are commonly associated with heart failure. The prognosis is poor and the hospital mortality high. The management of heart failure is an important consideration in allocating hospital resources in a district general hospital.
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PMID:Heart failure in a district general hospital. 842 54

Cardiovascular complications are among the most common and dangerous complications of cocaine abuse, ranging from episodic arrhythmias to myocardial infarction, strokes, cardiomyopathy, and sudden death. The central nervous system-mediated action of cocaine triggers an increase in circulating catecholamines, resulting in arterial vasoconstriction, increase in myocardial oxygen demand, myocardial ischemia, tachycardia, and other arrhythmias. The peripheral cardiovascular action of cocaine involves the inhibition of reuptake of catecholamines at adrenergic nerve terminals, with local release of epinephrine, direct stimulation and vasospasm of the coronary arteries, coronary intimal hyperplasia, inhibition of baroreceptors, interference with the electrical conduction through the myocardium, and direct myocardial toxicity. The cardiovascular complications of cocaine include cardiac dysrhythmias and hypertension, acute myocardial infarction, myocarditis, infectious endocarditis, ventricular dysfunction, dilated cardiomyopathy, hypotensive shock, and cerebral strokes. Cocaine-related vascular changes in the pregnant woman and fetus have been related to an increased incidence of abortion, abruptio placentae, and congenital anomalies of the fetus.
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PMID:Cardiovascular complications of cocaine abuse. 158 6

Fifty-four patients (18 males and 36 females, ages 2 to 37 years) with nonspecific aortoarteritis (NSAA) were studied. Evaluation revealed hypertension in 35, congestive heart failure (CHF) in 24, mild to moderate mitral regurgitation in six, and mild aortic regurgitation in two. Erythrocyte sedimentation rate was raised (greater than 35 mm in the first hour) in 38 patients. The arterial lesions included type I in seven, type II in eight, and type III in 34. Pulmonary artery involvement was present in 4 (type IV) of the 20 patients in whom it was studied. Selective coronary angiography was done in 11 patients and revealed 90% left main stenosis in one patient. Hemodynamic data revealed raised (greater than 7 mm Hg) mean right atrial pressure in nine, raised mean pulmonary artery pressure (greater than 20 mm Hg) in 29, and raised left ventricular filling pressure (greater than 12 mm Hg) in 27 patients. Radionuclide ventriculography revealed reduced (less than 45%) left ventricular ejection fraction (LVEF) in 27 patients. The myocardial morphology as evaluated on right ventricular endomyocardial biopsy revealed normal histology in nine, features of inflammatory myocarditis in 24, and nonspecific changes suggestive of dilated cardiomyopathy in six patients. Marked right ventricular endocardial thickening was present in three. All patients with CHF had some histologic abnormality. We emphasize that myocardial involvement including myocarditis is common in NSAA and may precipitate CHF in these patients.
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PMID:Cardiac involvement in nonspecific aortoarteritis (Takayasu's arteritis). 168 19

It is claimed that long-term treatment with beta-blockers improves cardiac function and exercise capacity in patients with various forms of congestive heart failure. This was first reported by Waagstein and coworkers in patients with idiopathic dilated cardiomyopathy in 1975 and was later confirmed in 8 further studies in this type of patient. A total of 211 patients with idiopathic dilated cardiomyopathy were treated for 12-19 months. About two thirds of the patients have improved to some extent. Seven other studies reported favourable long-term effects of beta-blockers in 120 patients with other forms of dilated cardiomyopathy, e.g. caused by coronary artery disease, adriamycin, diabetes, or valvular heart disease. Pooled data from 10 studies on 153 patients with various forms of cardiomyopathy, showed that ejection fraction was improved by 40% from 27 to 38%. Only two studies were inconclusive, both with only one month's treatment. In all studies with favourable effects of long-term beta-blockade, treatment was given for more than 2 months and in most cases for about 6 months. A number of beta-blockers have been used in the studies, including acebutulol, alprenolol, bucindolol, labetalol, metoprolol, practolol and propranolol. In most cases, a rather low dose was given initially and there was a stepwise increase in the dosages. After 6-8 weeks most patients were given beta-blockers in daily doses comparable to those given in patients with angina pectoris and hypertension. There is at present no indication that one beta-blocker is superior to others. It therefore seems reasonable to believe that the effects are due to beta 1-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New therapeutic strategies in chronic heart failure: challenge of long-term beta-blockade. 168 18

Up to now only 30 to 40% of patients who die suddenly can be identified as likely candidates before the event. Risk factors in these asymptomatic subjects include a familial history of coronary artery disease, high blood cholesterol levels, hypertension, smoking and, more importantly, an abnormal ECG at rest or during exercise. The predictive value of these abnormalities is too low to justify more detailed clinical investigations in most of these asymptomatic subjects. Exceptions might be the group of patients with multiple risk factors and competitive sportsmen. Sudden cardiac death is a well known complication in patients with hypertrophic and dilated cardiomyopathy. Risk factors in hypertrophic cardiomyopathy include a familial history of this disease, syncope and increasing age. Furthermore, in the adult, the presence of nonsustained episodes of ventricular tachycardia during Holter monitoring seems to indicate an increased risk of sudden cardiac death. In idiopathic dilated cardiomyopathy, the presence of frequent episodes of ventricular pairs and/or episodes of ventricular tachycardia during Holter monitoring, together with a reduced left ventricular ejection fraction, characterises the patient at risk of sudden cardiac death. In patients with coronary artery disease, the patient at risk of sudden cardiac death can be identified by investigating the following: coronary anatomy; global and regional left ventricular function; the presence of ischaemia during rest and/or exercise; the presence of late potentials, by means of the signal-averaged ECG; the presence of spontaneous ventricular arrhythmias (especially sustained and nonsustained ventricular tachycardia); and the results of electrophysiological testing. On the basis of these investigations, 3 subgroups can be distinguished: patients at low risk, medium risk, and high risk of sudden cardiac death.
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PMID:Can we predict sudden cardiac death? 171 71


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