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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using new techniques, we quantitated left ventricular myocardial fiber hypertrophy and interstitial tissue in four groups of autopsied hearts free of coronary disease: 1) 22 normal hearts, 2) 20 hearts from patients with mitral incompetence (NYHA Class II-III) who died early after mitral valve replacement from causes other than cardiac failure, 3) 22 hearts from patients with mitral incompetence (NYHA Class III-IV) who died early after mitral valve replacement from cardiac failure with low cardiac output syndrome, and 4) 22 hearts from patients with hypertensive heart disease (NYHA Class II-III). Myocardial fiber hypertrophy was quantitated by measuring cross-sectional myocardial fiber diameter; the proportion of interstitial tissue was quantitated by using a computerized, high-resolution video image-digitizing system. Myocardial fiber average diameter in groups 2, 3 and 4 was significantly higher than group 1. The proportion of interstitial tissue was significantly increased in group 3. In chronic mitral incompetence an increase in left ventricular interstitial tissue may play a role in the development of severe cardiac failure.
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PMID:Quantitation of left ventricular myocardial fiber hypertrophy and interstitial tissue in human hearts with chronically increased volume and pressure overload. 13 91

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.
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PMID:Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta. 14 28

A phonocardiological analysis of the first heart sound was made and systolic time intervals were measured in 40 patients (ischaemic heart disease, hypertensive heart disease, cardiomyopathies) with incipient cardiac failure (functional groups I--II according to the NYHA) with auscultatory changes of the first heart sound and in controls of randomly selected healthy persons or patients in whom cardiopulmonary disease was excluded. The patients in all diagnostic groups differed significantly (P less than 0.05--0.001) in practically all the phonocardiographic indicators from the controls. The most constant abnormal finding was a pathological split of the first heart sound which may be divided into three phonocardiographic forms. Simultaneously, systolic time intervals alterations (P less than 0.02--0.001) were also found in these patients and indicated a lowered performance of the left ventricle. The results suggest that 1) a certain relation exists between systolic time intervals and the phonocardiographic pattern of the first heart sound in patients with cardiovascular diseases and those without it; 2) the modified (pathologically splitted and prolonged) first heart sound could be a sign of incipient cardiac failure.
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PMID:The first heart sound abnormalities accompanied with alteration of systolic time intervals in incipient heart failure. 53 4

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67

Coronary hemodynamics (blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical hypertension. Significantly reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Medial hypertrophy of small coronary vessels associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impaired coronary flow in hypertensive left ventricular hypertrophy. After long-term pharmacotherapy, there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible rational approach to the prevention of cardiac failure in hypertensive patients. Controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.
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PMID:Coronary vascular changes in the progression and regression of hypertensive heart disease. 172 Apr 80

In essential hypertension, ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal, even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). One of the profound mechanisms influencing both myocardial and coronary function in hypertensive heart disease is the pressure-dependent development of smooth vascular hypertrophy (media) or coronary resistance vessels. Consequently, the oxygen supply to the myocardium is impaired and secondary lesions occur such as fibrosis, increased myocardial and perivascular collagen content and scars within the heart muscle. Diastolic dysfunction develops, as well as an increase in myocardial stiffness, thus promoting the transition from the concentric (compensated) to the eccentric or dilated (decompensated) state, with the consequence of the occurrence of cardiac failure. On the basis of both functional and morphological criteria, evidence is presented in this report that coronary small vessel disease is one of the underlying mechanism for the development of cardiac failure in hypertensive heart disease.
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PMID:Development of cardiac failure by coronary small vessel disease in hypertensive heart disease? 183 64

Left ventricular (LV) systolic function was assessed in patients with hypertensive heart disease (HHD, n = 30), hypertrophic cardiomyopathy (HCM, n = 27), dilated cardiomyopathy (DCM, n = 25), volume overload heart (VOH, n = 31) and normal subjects (NS, n = 32) in the two-dimensional framework of force-length (end-systolic stress-end-systolic volume index) and stress-shortening (mid-systolic stress-ejection fraction). Quadratic discriminant analysis revealed that the ellipses of confidence of HHD and normal subjects were in the same place with regard to both force-length and stress-shortening, while all other groups were well-discriminated. Three subgroups of patients, those with DCM with mild heart failure and those with VOH (with and without heart failure), were easily distinguishable on the basis of stress-shortening, but not on the basis of force-length measurements. It is concluded that LV systolic function and afterload are maintained within the normal range under pressure and volume overload until symptoms of heart failure appear via the mechanism of compensatory hypertrophy. Stress-shortening appears to be a more useful parameter than force-length for the analysis of LV systolic function in clinical practice.
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PMID:Clinical assessment of left ventricular systolic function by force-length and stress-shortening relationships. 203 May 47

The association between proteinuria and congestive cardiac failure was investigated in patients with hypertensive heart disease, cardiomyopathy, rheumatic heart disease and cor pulmonale. In 33 such patients, proteinuria occurred before and after successful treatment of the cardiac failure. Overall there was a wide variation in the degree of proteinuria amongst the various groups and statistical analysis showed that the distribution of levels of proteinuria and the mean levels of proteinuria were statistically different between any two groups of patients, P = 0.05. Biopsy proven hypertensive nephrosclerosis was found to be a cause of heavy proteinuria which was in the nephrotic range in two such patients. Congestive cardiac failure due to hypertensive heart disease should be included in the differential diagnosis of massive proteinuria even in the absence of renal insufficiency.
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PMID:The pattern of proteinuria in congestive cardiac failure due to common heart diseases. 206 87

Coronary hemodynamics (coronary blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical essential hypertension. Significant reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Extracoronary reasons for these phenomena were ruled out. Considerable thickening of the coronary resistance vessels (medial hypertrophy) in hypertensive hypertrophy associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impairment of coronary flow. After long-term pharmacotherapy there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible approach to the rational prevention of cardiac failure in hypertensive patients. For future investigations, controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.
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PMID:Significance of coronary circulation in hypertensive heart disease for development and prevention of heart failure. 213 55


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