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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

All autopsies on Black patients who died of heart disease at Baragwanath Hospital were examined for the years 1959, 1960 and 1976. The commonest form of heart disease encountered in South African Blacks is undoubtedly hypertensive heart disease and by far the majority of these cases are of essential hypertension. There appears to have been a slight rise in the incidence of hypertension. Rheumatic heart disease is extremely common, and affects young people, who often have advanced valvular lesions by puberty. The incidence of idiopathic cardiomyopathy does not seem to have altered materially, although there has perhaps been a slight drop, which may be accounted for by the tendency of clinicians to place cases of congestive cardiac failure with mild hypertension in the hypertensive group rather than in the idiopathic cardiomyopathy group. There was a significant alteration in the incidence of myocardial infarction; in 1959 and 1960 these cases comprised less than 1% of all cardiac deaths but in 1976 they comprised nearly 12%. There has also been a dramatic fall in the incidence of cardiovascular syphilis.
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PMID:The changing pattern of heart disease in South African Blacks. 60 91

In this review, the coronary haemodynamics of hypertrophic heart disease are discussed with reference to data published over the last 15 years. Coronary reserve is reduced in the presence of concentric cardiac hypertrophy, but is similar to normal in hypertrophic obstructive cardiomyopathy and aortic stenosis, despite marked left ventricular hypertrophy. A moderate decrease in coronary reserve is found in aortic incompetence and in dilated essential hypertension. In hypertensive heart disease, improvement in coronary reserve can be achieved by long-term vasodilator therapy.
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PMID:Left ventricular hypertrophy, myocardial blood flow and coronary flow reserve. 130 Dec 55

To assess the role of arterial hypertension in left ventricle (LV) hypertrophy among hemodialysis patients, echocardiographic evaluation was performed in 10 hypertensive and 13 normotensive hemodialysis subjects matched for age, sex, race, duration of dialysis treatment and degree of interdialytic volume expansion. We excluded from the latter group patients with previous hypertension since hypertensive heart disease may persist after adequate blood pressure control. We also studied 17 normal controls and 10 non-uremic patients with essential hypertension. Comparisons between the two uremic groups showed that the hypertensive patients had a higher mass index (222 +/- 74 x 108 +/- 26, p = 0.0001) and posterior wall thickness (12 +/- 2 x 9 +/- 2, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 +/- 0.7 x 5.8 +/- 1, p = 0.0001). There were no significant echocardiographic differences between normal controls and normotensive uremics. In contrast, compared to controls, hypertensive uremic patients showed an increased LV mass index (222 +/- 74 x 83 +/- 21, p = 0.0001) and posterior wall thickness (12 +/- 2 x 7 +/- 1, p = 0.0001) and a reduced LV radius/wall thickness ratio (4.4 +/- 0.7 x 6.5 +/- 1.1, p = 0.001), characterizing concentric hypertrophy. They also had ventricular dilation with larger LV dimensions than in controls (53 +/- 5 x 47 +/- 4, p = 0.004). In patients with essential hypertension, the mass index (135 +/- 22), wall thickness (11 +/- 1) and LV radius/wall thickness ratio (4.3 +/- 0.7) significantly differed (p = 0.0001) from those in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of arterial hypertension in left ventricle hypertrophy in hemodialysis patients: an echocardiographic study. 138 45

To determine whether myocardial ischemia is accompanied by variation in heart rate and/or blood pressure, ST-segment analysis on Holter-ECG and ambulatory blood pressure monitoring was performed in 78 patients (64 males/14 females) with essential hypertension. Thirteen out of 55 patients (24%) with angiographically proven coronary artery disease (CAD) showed ST-segment depression (ST-D; group A pos). We observed 41 ST-D (1-11 ST-D; median: 2) lasting from 1 min to 70 min 15 s (median: 4 min 42 s) and an average depression of 185 +/- 48 mV. In comparison, in 6 of 23 patients (26%) with a normal angiogram 24 ST-D (1-10; median: 3; group B pos), which showed longer duration (1 min to 109 min 20 s; median: 11 min 10 s) and less depression (137 +/- 47 mV) have been found. 73.3% of all ST-D in group A pos and all in group B pos were preceded by an average increase in heart rate of 13 bpm. Exclusively, 12 episodes of ischemia (29.3%) in patients with CAD and 8 (33.3%) in patients without CAD were accompanied by an increase in blood pressure, which was more distinct in group A pos. Transient myocardial ischemia can be shown in hypertensive heart disease unrelated to CAD. A clear correlation between an increase in blood pressure and ST-D could not be proven.
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PMID:[Blood pressure variability and transient myocardial ischemia in patients with essential hypertension]. 151 10

In arterial hypertension, casual blood pressure seems to be weakly related to the level of cardiac involvement. The aim of the present study was to assess if blood pressure during ambulatory monitoring, and during different stress tests, is a stronger predictor of anatomical and functional changes observed in hypertensive heart disease. To this aim, 29 untreated patients with borderline-to-moderate essential hypertension underwent an echo-Doppler evaluation to determine left ventricular thickness and mass. From transmitral flow, the ratio between late and early filling velocities (A/E ratio) was used to assess left ventricular diastolic behaviour. On the same day that ultrasonic study was carried out, we also measured a set of casual blood pressures; conducted a mental arithmetic test (standardized series of mental subtractions); a handgrip test (30% of maximum voluntary contraction for 3 minutes); and performed noninvasive ambulatory monitoring of blood pressure (Spacelabs 5200). Significant relationships were observed between left ventricular mass and both night-time systolic blood pressure (r = 0.46, P less than 0.02) and peak systolic blood pressure during mental stress (r = 0.39, P less than 0.05). The A/E ratio was significantly associated with casual systolic and diastolic blood pressure (r = 0.45, P less than 0.02; r = 0.38, P less than 0.05, respectively); day-time diastolic blood pressure (r = 0.47, P less than 0.02); night-time systolic and diastolic blood pressure (r = 0.44, P less than 0.05; r = 0.42, P less than 0.05 respectively); and peak systolic blood pressure during the mental arithmetic test (r = 0.44, P less than 0.05). Our results seem to confirm the presence of a relationship between causal blood pressure and left ventricular filling. Moreover, the transmitral flow seems to be dependent on both mean levels of blood pressure on ambulatory monitoring and systolic blood pressure during mental stress. As concerns left ventricular mass, the correlations observed support the weakness of the links between blood pressure and left ventricular anatomy.
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PMID:Casual, ambulatory and stress blood pressure: relationships with left ventricular mass and filling. 183 35

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

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

The sensitivity of echocardiographically derived left ventricular mass in predicting morbidity in essential hypertension has led to widespread use of this measurement in cross-sectional studies to assess the pathophysiology of hypertensive heart disease. Over the past decade, a variety of studies in hypertensives have evaluated the blood pressure determinants of both the structural and the functional aspects of left ventricular hypertrophy. Recent data presented here demonstrate that average daily blood pressure derived from non-invasive ambulatory blood pressure monitoring is superior to casual blood pressure in predicting an increased left ventricular mass index and left atrial dimension, and altered left ventricular systolic and diastolic function. Further data analysis in previously untreated mildly hypertensive subjects (diastolic blood pressure less than 140/90 mmHg) showed that the average daily pressure load (defined as the percentage of blood pressure values greater than 140/90 mmHg while awake and greater than 120/80 mmHg during sleep) delineates groups at high and low risk of developing hypertensive heart disease.
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PMID:Predicting hypertensive heart disease via non-invasive methodology: relationship between ambulatory blood pressure and cardiac indices derived by echocardiography and radionuclide ventriculography. 215 May 31

Various haemodynamic functions were studied in 70 patients (51 men and 19 women; mean age 53.0 +/- 7.0 years) with essential hypertension. The following parameters were measured, at rest and on exercise: systolic and diastolic blood pressure, heart rate, mean pulmonary artery pressure, cardiac output and peripheral vascular resistance. 15 normotensive subjects (11 men and four women; mean age 54.4 +/- 7.2 years) without significant cardiovascular disease served as controls. Resting peripheral vascular resistance (PAP) in the hypertensives was, at 1634.7 +/- 239.0 dyn/s.cm-5, higher by 41%, on exercise at 1029.4 +/- 105.9 higher by 14%, than in the controls (at rest 1157.1 +/- 118.9 dyn/s.cm-5, on exercise 706.9 +/- 94.1 dyn/s.cm-5; P less than 0.0001). Cardiac output at rest was 9.6% lower, on exercise 8.0% lower than in the controls (neither change significant). Thus the increased peripheral vascular resistance was the sole cause of the increased blood pressure. Mean PAP, as a measure of left-ventricular filling pressure, in hypertensives was 14.7 +/- 3.9 mm Hg at rest, 34.9 +/- 7.8 mm Hg on exercise, an increase of 14% and 40%, respectively, over the control values of 12.7 +/- 1.9 mm Hg at rest and 24.4 +/- 2.8 mm Hg on exercise (P less than 0.0001). The raised left-ventricular filling pressure is an indication of early hypertensive heart disease.
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PMID:[Resting and exercise hemodynamics in essential arterial hypertension]. 229 31


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