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

Left ventricular function was evaluated prospectively during 1 year in a controlled clinical study of 73 patients with chronic obstructive lung disease. The control group comprised 68 patients matched for age and sex and with no evidence of airways obstruction. Left ventricular hypertrophy was found in 52% and systemic hypertension in 58% of patients in the study group compared with 6% and 15% respectively in the controls. Left ventricular hypertrophy was diagnosed in 70% of patients with chronic bronchitis and in 19% of those with chronic emphysema. Systemic hypertension was observed in 45% of the bronchitic type patients and in 81% of those with emphysema. The incidence of myocardial infarction in the study group was not lower than in the controls. The high frequency of left ventricular hypertrophy in patients with chronic obstructive lung disease can probably be related to a similar high frequency of systemic hypertension. Hypertension per se does not explain left ventricular hypertrophy in all patients with chronic bronchitis, but hypoxemia and acidosis seem to be of pathogenetic importance in these cases.
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PMID:Systemic hypertension, left ventricular hypertrophy and myocardial infarction in patients with chronic obstructive lung disease. 14 14

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

In this study naturally occurring hypertension in wild rhesus monkeys has been noted with a frequency of 13 out of 428 monkeys examined. The maximum systolic/diastolic blood pressure was 242/140 mm of Hg. Clinically there was evidence of grade I retinopathy in one case only, otherwise the animals did not manifest any symptom to suggest illness. Biochemical examination revealed normal plasma angiotensin activity but the level of serum sodium was slightly elevated. The serum potassium, blood urea and serum creatinine values were within normal limits. Serum cholesterol was, however, elevated in two cases. All hypertensive animals were sacrificed by exsanguination and a complete autopsy was performed. It revealed left ventricular hypertrophy in almost all cases, patchy myocardial degeneration with fibrosis in 3 animals and advanced renal disease only in 3 cases. It therefore appears that most of these cases of hypertension belonged to the idiopathic group.
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PMID:Spontaneously occurring hypertension in wild Rhesus monkeys. 15 Nov 70

Great ECG changes (Frank system) with age were found in normal men. ECG diagnostic criteria valid in Romania were studied by multivariate analyses in men aged 40--60 suffering from hypertension (Hyp) without cardiac congestive failure (CCF), out of which one group with left ventricular hypertrophy (LVH) and another one without it. Echocardiographic studies in normal and hypertensive men past forty, as well as studies in experimental Hyp with LVH and without CCF were carried out. Heart X-ray evaluation is not a functional one. Some non-invasive methods in men do not determine an accurate evaluation of LV performance. The increase of LV muscular mass alone cannot explain the ECG changes in LVH in Hyp without CCF. Two conditional adaptive mechanisms: the liberation of catecholamines from the myocardium storage, induced by the pressure overload stress, and the increase of intracellular Ca++ influx could contribute to the respective ECG changes.
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PMID:Studies concerning the significance of orthogonal ECG changes with age in normal men and in arterial hypertension without congestive cardiac failure in men past forty. 15 76

We examined the pulmonary vascular reactivity of normotensive rats (NR) and spontaneously hypertensive rats (SHR) to acute and chronic pressor stimuli. In rats kept at low altitude (1,520 m), SHR had a slight degree of right ventricular hypertrophy, but there was no difference between SHR and NR in either right ventricular systolic pressure or pulmonary artery wall thickness. When compared to blood-perfused lungs from low altitude NR, lungs from low altitude SHR were normoresponsive to acute airway hypoxia, hyporesponsive to intra-arterial angiotensin II, and hyperresponsive to intra-arterial prostaglandin F2alpha. After exposing rats to simulated high altitude (4--6 weeks at 4,270 m) to induce hypoxic pulmonary hypertension, SHR had a higher right ventricular systolic pressure, a greater degree of right ventricular hypertrophy, and more pulmonary artery medial thickening than did NR. The results indicate that although the pulmonary vasculature of SHR does not become hypertensive spontaneously, it might have an increased tendency to develop hypertension when exposed to an appropriate stimulus, i.e., chronic airway hypoxia.
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PMID:Pulmonary vascular reactivity in the spontaneously hypertensive rat. 15 32

Septal and left ventricular posterior wall (LVPW) thicknesses and their ratios were studied at the left ventricular outflow tract and left ventricular cavity in 66 patients with echocardiographically diagnosed left ventricular concentric hypertrophy, 20 with idiopathic hypertrophic subaortic stenosis (IHSS), and 34 normal subjects. Concentric hypertrophy was due to hypertension in 41 subjects and to valvular disease in 15 subjects. Septal thickness in normal subjects was related to body surface area (p less than 0.02). In 12% of normal subjects, 39% of patients with concentric hypertrophy and 95% with IHSS, the septal/LVPW ratio was greater than or equal to 1.3. Thirty-two percent of patients with hypertension, 78% with aortic stenosis, and 60% with aortic insufficiency had septal/LVPW ratios greater than or equal to 1.3 at left ventricular midcavity level. In conclusion, a septal/LVPW thickness ratio of greater than or equal to 1.3 is common in patients with concentric left ventricular hypertrophy and may also occur in normal subjects. A ratio greater than or equal to 1.5 may be more specific for genetically determined asymmetric septal hypertrophy.
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PMID:Interventricular septal thickness and left ventricular hypertrophy. An echocardiographic study. 15 45

Although many ECG criteria exist for diagnosis of left ventricular hypertrophy (LVH) in hypertensive man, little is known of which specific ECG changes accompany progression of LVH with duration of hypertension. The spontaneously hypertensive rat (SHR) provides the best animal model thus far developed for studying this process since these animals demonstrate a progressive increase in left ventricular/body weight ratio with age. Electrocardiograms were performed under light ether anesthesia in four age groups of SHR and two normotensive Wistar strains (NR and WKY). Analysis of variance for two factors (rat strain and age) revealed progressively increased QRS and P-wave duration and delay in intrinsicoid deflection in SHR (p less than 0.001). Bipeak P-wave notching was also noted in SHR similar to left atrial abnormality in hypertensive man. Thus, specific ECG indices can be identified in association with the known progressive increase in left ventricular mass in SHR and should provide a better means to understand evolving ECG changes in LVH.
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PMID:ECG alterations with progressive left ventricular hypertrophy in spontaneous hypertension. 15 96

For many years clinicians have suspected that hypertrophied ventricles have an inadequate coronary circulation. Recent studies have confirmed early observations that flow per gram in hypertrophied ventricles is normal at rest. However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Studies that have employed labeled microspheres to assess regional myocardial perfusion have shown that the transmural distribution of myocardial perfusion is often abnormal in dogs with left ventricular hypertrophy. In addition, studies of cardiac hypertrophy in many animal models have shown that maximal coronary vasodilatation is limited substantially. Furthermore, when hypertrophied hearts are subjected to a physiologic stress that induces coronary vasodilatation, endocardial underperfusion occurs frequently. Thus, studies in animals suggest that cardiac hypertrophy adversely affects the coronary circulation. The availability of new techniques for estimating phasic and transmural coronary blood flow in man should make it possible to extend these studies to patients with cardiac hypertrophy.
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PMID:Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation. 15 62

Increased arterial pressure is obviously the major stimulus to cardiac hypertrophy in hypertension. However, different studies suggest that in addition to the pressure load, other factors could play participating roles in determining the degree of ventricular hypertrophy in response to the hypertensive disease as well as the degree of its reversal after control of arterial pressure. These other mechanisms include genetic factors and concimitant processes such as aging and the presence of cardiomyopathy or other disease. Two neurohumoral influences, namely, the adrenergic and the renin-angiotensin systems, may also participate, and the early evidence supporting these possible contributing factors is cited. Further studies are needed to determine the relative importance of each of these factors in different types of hypertension and in their response to different modes of antihypertensive therapy.
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PMID:Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy? 15 71

M-mode echocardiography was performed in 81 patients with chronic arterial hypertension in order to determine the specificity and sensitivity of the various ECG criteria used for diagnosing left ventricular hypertrophy (LVH) in the determination of left ventricular wall thickening (LVWT). Fifteen popular ECG criteria were studied and showed to be highly specific for LVWT (90 percent to 100 percent). TV1 greater than TV6, RV8 greater than 20 mm and SV1 + Rmax V5 or V6 greater than 35 mm were the most sensitive criteria (69 percent, 54 percent, and 52 percent respectively). The popular limb lead criteria for LVH were less sensitive than the precordial lead criteria in the determination of LVWT. The Estes point system, although less sensitive than some of the other voltage criteria, showed an absolute specificity for LVWT. The ST segment deviation with strain pattern was found in 46 percent of patients with LVWT. An isolated ST segment deviation without any other voltage criterion reflected at most only mild wall thickening. Six patients with LVWT had normal ECG; all of them were categorized in the mild LVWT group. Left axis deviation was found to be a poor indicator of wall thickening in uncomplicated hypertensive patients.
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PMID:Determination of left ventricular wall thickening in patients with chronic systemic hypertension. Correlation of electrocardiography and echocardiography. 15 58


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