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

In order to investigate the mechanism and treatment of angina decubitus, 20 patients (18 men and 2 women aged 36-70 years) were studied during hospitalization. All patients were found to have an increased heart rate x systolic blood pressure product before the onset of angina decubitus, indicating that this type of angina pectoris belongs to the category of effort angina. Of the 11 patients investigated by continuous hemodynamic monitoring, 3 had significant progressive increases in pulmonary artery systolic pressure (PASP) and pulmonary artery diastolic pressure (PADP) before onset: their episodes of angina could not be completely controlled by digoxin and diuretics, but quickly subsided after beta blockers were added. Among the other 8 patients, PADP increased slightly in 5 and remained unchanged in 3 cases before onset: these patients had no manifestations of LV dysfunction, and beta blockers combined with coronary vasodilators produced satisfactory effects. These results indicate that LV failure is not a major factor in the pathogenesis of angina decubitus. The LV diastolic dysfunction seen in 8/11 cases may have been related to LV hypertrophy caused by long-term hypertension or chronic persistent ischemia.
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PMID:Hemodynamic observation and treatment approach for patients with angina decubitus. 136 74

We evaluated the effects of a single oral dose of 5 mg of isradipine compared to placebo in a randomized, double-blind, crossover study using gated radionuclide angiography at rest and during exercise in 20 patients with stable chronic angina. Isradipine improved both anginal symptomatology and ST-segment depression during exercise, with a concomitant favorable effect on the isotopic parameters exploring systolic and diastolic left ventricular function. There was a marked increase of the ejection fraction during exercise with isradipine compared to placebo (61 +/- 14% vs. 55 +/- 15%, respectively, p less than 0.001) as well as a significant improvement in the peak ejection rate and the peak filling rate at rest [2.56 +/- 0.62 vs. 2.16 +/- 0.54 end diastolic volume (EDV) per second and 2.14 +/- 0.59 vs. 1.87 +/- 0.37 EDV/s, respectively] and during exercise (3.49 +/- 0.97 vs. 3.10 +/- 1.07 EDV/s and 4.05 +/- 1.34 vs. 3.65 +/- 1.25 EDV/s, respectively). We conclude that isradipine has a beneficial effect on the clinical and electrocardiographic signs of exercise-induced ischemia, leading to a significant improvement of the systolic and diastolic parameters of left ventricular function. Therefore, isradipine is potentially a useful treatment for patients with exertional angina and hypertension, alone or associated with beta blocker medication.
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PMID:Effects of oral isradipine on left ventricular function at rest and during exercise in patients with stable chronic angina: a double-blind, placebo-controlled crossover study. 137 79

Hypertension causes vascular changes of essentially three types: structurally adaptative changes, degenerative alterations unrelated to atherosclerosis, and atherosclerosis. Structural changes result in an increased peripheral resistance, even in the relaxed vascular bed, and a reduced collateral capacity, thus predisposing to ischemia distal to an arterial stenosis/occlusion and to "watershed" infarcts in connection with a drop in blood pressure. Degenerative changes in the small intracerebral arteries can lead to plasma extravasation and focal brain edema, lacunar infarcts, and intracerebral hemorrhages. Hypertension also predisposes to saccular aneurysms and subarachnoid hemorrhages. Finally, atherosclerotic changes including stenoses or occlusions of predominantly extracranial and pial arteries give rise to transitory ischemic attacks and brain infarcts by artery-to-artery embolism or distal hemodynamic perfusion insufficiency.
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PMID:Vascular mechanisms in hypertensive cerebrovascular disease. 137 27

Carvedilol is a multiple-action cardiovascular agent that is both a beta-adrenoceptor antagonist and a vasodilator and has recently been made available for the treatment of mild-to-moderate hypertension. Clinical trials are ongoing to establish the efficacy of carvedilol in angina and congestive heart failure. beta-Adrenoceptor antagonists are known to reduce myocardial work secondary to reductions in heart rate and contractility; accordingly, they have been shown to be cardioprotective in animals and in humans. Because carvedilol has beta-adrenoceptor antagonist activity, it also should provide significant cardioprotection. The additional vasodilating activity of carvedilol, which will further reduce myocardial work by decreasing afterload and myocardial wall tension, should provide more salvage of ischemic myocardium than that afforded by a pure beta-adrenoceptor antagonist, such as propranolol. We investigated the ability of carvedilol and propranolol to reduce infarct size in experimental models of acute myocardial infarction in the rat, pig, and dog. The left anterior descending coronary artery was occluded for 30 (rat) or 45 min (pig) and then reperfused for 24 h (rat) or 4 h (pig). In the dog, the left circumflex coronary artery was occluded for 60 min and reperfused for 24 h. Vehicle, carvedilol, or propranolol was administered intravenously 15 min before ischemia (and, in the rat only, repeated 4 h after ischemia). An additional group of dogs was subjected to permanent left anterior descending coronary artery occlusion for 6 h, and carvedilol or propranolol was given 15 min after occlusion. Infarct size was examined on stained tissue sections using quantitative image analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection with carvedilol. 137 42

A review is given of the normal regulation of cerebral blood flow (CBF) and its pathophysiology in hypertension and stroke. In otherwise healthy hypertensive patients, the absolute level of CBF is the same as in normal subjects. CBF autoregulation, however, is shifted towards higher pressure, thus impairing the tolerance to hypotension. In most patients, this does not interfere with the beneficial effect of treatment, i.e., stroke prevention. Cerebral ischemia, however, may be provoked by overzealous pressure lowering in selected clinical settings: initial or intensified treatment of very severe hypertension, treatment of hypertension in the elderly, and treatment of hypertension in acute stroke. In the latter, a complicated sequence of brain ischemia and hyperemia makes antihypertensive intervention difficult in the early phase, when blood pressure is probably best allowed to decrease spontaneously.
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PMID:Regulation of cerebral blood flow in health and disease. 138 71

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

Cocaine abuse may lead to serious cardiac complications, including myocardial ischemia and infarction, myocarditis, cardiomyopathy and arrhythmias. With concomitant use of alcohol and cocaine, cocaethylene is produced by hepatic transformation. Cocaethylene is now thought to be primarily responsible for the deaths that occur among cocaine abusers. Treatment of cardiovascular complications focuses on cocaine-induced ischemia, hypertension and arrhythmias. The use of thrombolytic agents in myocardial infarction remains controversial. Concurrent detoxification with bromocriptine and norepinephrine is recommended.
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PMID:Cardiovascular complications of cocaine abuse. 846 3

The aim of this study was to clarify how collagen deposition or medial hypertrophy of the vascular wall affects the coronary dilator reserve in pressure-overloaded hearts and whether inhibition of collagen deposition reverses the abnormalities after relief of pressure overload. We used ascending aortic banding and debanding methods and superimposed beta-aminopropionitrile in some of the banded rats (50 mg/kg i.p., twice a day). Ten weeks of banding increased in vivo peak systolic left ventricular pressure and produced medial hypertrophy, an increase in collagen deposition in the myocardial and perivascular tissues, and myocardial hypertrophy in the banded group without beta-aminopropionitrile treatment. Superimposition of beta-aminopropionitrile treatment on banding inhibited the increase in collagen deposition. In the groups debanded after the 10-week banding period, both with and without beta-amino-propionitrile treatment, medial and myocardial hypertrophy regressed 4 weeks after debanding. We estimated coronary dilator reserve in Langendorff preparations perfused with modified Tyrode's solution containing oxygenated bovine red blood cells and serum albumin. The ratio of reactive peak flow after brief ischemia-to-resting flow decreased in both of the banded groups. After debanding, the ratio remained lower in the banded group without beta-aminopropionitrile treatment than in the control group. However, debanding in the group with beta-aminopropionitrile treatment increased the ratio to a level similar to that of the control group. Thus, in pressure-overloaded cardiac hypertrophy with coronary hypertension, coronary reserve seems to be determined by medial hypertrophy independently of collagen deposition, but collagen deposition plays an important role in the reversal of vasodilator reserve after relief of the overload.
Hypertension 1992 Oct
PMID:Collagen deposition and the reversal of coronary reserve in cardiac hypertrophy. 139 84

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

In 1983-1988, the results of conservative and surgical treatment of patients with atherosclerotic ischemia of the lower limbs were assessed with the aid of a questionnaire. A possibility of prognosis was assessed with the use of mathematically processed data obtained with such approach. An effect of clinical symptoms (intermittent claudication distance, resting pain, necrosis) and stage of the disease (duration, K/R index) and risk factors (blood cholesterol, triglycerides, diabetes mellitus, ischemic heart disease, arterial hypertension) on the result of surgical treatment was analysed. The obtained results suggest that clinical symptoms and risk factors may predict the results of surgical treatment in the atherosclerotic ischemia of the lower limbs.
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PMID:[Anticipated results of arterial surgery in chronic atherosclerotic ischemia of the lower limb]. 140 53


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