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

To determine the factors associated with low-output left ventricular failure (LVF) in endstage renal disease (ESRD), we performed echocardiography and gated cardiac scan on 217 nondiabetic dialysis and transplant patients. The prevalence of low-output LVF (ejection fraction less than 55% and left ventricular end diastolic diameter greater than or equal to 5.5 cm) in dialysis patients was 18% and in transplant patients 2%. The 26 patients with LVF were compared to 52 controls without LVF, matched by age, sex and year of starting treatment for ESRD, but not for current ESRD therapy. Mean age was 55 +/- (SEM) 14 years; 73% of the patients in both groups were males. Duration of treatment for ESRD was 5.6 +/- 4.3 years in patients, compared to 5.1 +/- 4.1 years in controls. Significant differences between LVF patients and controls included current treatment (73% of cases were on hemodialysis and 8% were transplanted, compared to 48 and 42%; chi 2 = 9.9, p less than 0.01), high serum creatinine, smoking and high serum alkaline phosphatase. There were no differences for current blood pressure, proportion on treatment for hypertension, left ventricular wall thickness, symptomatic ischemic heart disease, proportion with functioning vascular access, degree of weight gain between dialyses, hemoglobin level or high transfusion requirement. Multiple logistic regression demonstrated the most significant and independent variables associated with LVF were high alkaline phosphatase (suggestive of hyperparathyroidism), smoking and high serum creatinine levels (reflecting degree of uremia). Dialysis patients with LVF (n = 23) were compared to dialysis patients who had normal echocardiograms (n = 29).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-output left ventricular failure in end-stage renal disease. 330 13

In hypertensive patients, morbidity and mortality from the malignant phase, stroke, left ventricular failure, coronary disease and progressive renal failure are closely linked to the level of blood pressure. This relationship between blood pressure and risk can be demonstrated also when blood pressure is lowered with antihypertensive agents. Thus, it appears that the treated blood pressure level is a much stronger indicator of prognosis than is the initial untreated value. However, in the last 2 years, 3 large scale studies have shown that morbidity and mortality in treated hypertensive patients are still considerably higher than expected and significantly greater than in comparable normotensive subjects or control populations. There could be several explanations for these disturbing findings. One is that long-standing hypertension may cause irreversible cardiovascular changes that continue to put such individuals at risk, even after their blood pressure has been brought under control. Another possibility is that the pharmacological agents used in the treatment of hypertension may have some partially adverse effects in addition to their beneficial action on blood pressure. For example, drug-induced changes in serum lipids or of serum electrolytes could somewhat offset the advantages from blood pressure reduction. Furthermore, less than optimal control of elevated blood pressure could be a factor. It is worth noting that consistent arterial pressure reduction has been achieved in only a fraction of treated patients in the large scale intervention trials.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is hypertension treated adequately? 344 56

Some calcium antagonist drugs used in hypertension and cardiac diseases have been shown to increase plasma digoxin levels mainly as a result of reduced renal clearance. Felodipine is a new dihydropyridine calcium antagonist drug with cardiovascular effects, whose pharmacokinetics and effects on plasma digoxin levels have been studied in patients with left ventricular failure. 12 patients (11 men) on long term digoxin therapy were given 2.5 or 5 mg felodipine bid for 7 days followed by 1 week on 10mg bid. Plasma levels of digoxin and felodipine were measured before dosage and 30, 60 and 90 minutes and 2, 3, 4, 6, 8, 10 and 24 hours after the first dose and after 1 week of therapy (steady state). The area under plasma concentration versus time curve was calculated after the first dose and in steady state both for digoxin and felodipine. The absorption characteristics Cmax and Tmax were calculated both for felodipine and digoxin on the different felodipine doses. There was a linear relationship between dose and plasma level of felodipine. Plasma half-life in the 4- to 10-hour period of felodipine was 5.5 hours after a 10mg single dose, and 12 hours after 10mg bid. Felodipine 2.5mg, 5mg and 10mg all transiently increased peak plasma digoxin concentrations (by about 40%) at 1 hour after intake. Urinary excretion of digoxin during the day was unchanged, but impaired renal clearance may account for the transient increase in digoxin plasma level after felodipine.
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PMID:Pharmacokinetics of felodipine and effect on digoxin plasma levels in patients with heart failure. 344 63

Right atrial hypertension has been considered to have a major physiologic influence on the formation of transudative pleural effusions. Since pleural fluid is thought to be cleared primarily by the parietal pleural lymphatic vessels that empty into the systemic veins, systemic venous hypertension secondary to right atrial hypertension should decrease the lymphatic drainage of the pleural space. We retrospectively studied nine patients and prospectively studied 18 patients with long-term right atrial or pulmonary arterial hypertension (or both). All patients had stable respiratory symptoms, and none had a significantly elevated pulmonary arterial wedge pressure. Our purpose was to determine the relationship of right atrial and pulmonary arterial hypertension to the development of transudative pleural effusions. Posteroanterior and bilateral decubitus chest roentgenograms and ultrasound were used to detect pleural effusions. Pleural effusions were not identified in any of the 27 patients, even in four patients with right atrial pressures greater than 20 mm Hg. We conclude that chronic elevation of right atrial pressure or pulmonary arterial pressure (or both) alone is not a cause of pleural effusion. In contrast, elevation of left atrial and pulmonary arterial wedge pressures is associated with the formation of transudative pleural effusions in man. Thus, if pleural effusions are detected in patients who have cor pulmonale, a search should be made for coexisting left heart failure or a primary cause of pleural inflammation, such as pulmonary emboli or infection.
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PMID:Lack of association of pleural effusion with chronic pulmonary arterial and right atrial hypertension. 367 41

Nicardipine is a new slow channel calcium blocker. It has been shown to be effective in the treatment of hypertension and angina pectoris. Nine patients with mild to moderate left ventricular failure were given intravenous infusions of nicardipine and the haemodynamic effects measured. In patients receiving 20 mg of nicardipine, mean cardiac index rose to a peak 1.81 X min-1 X m-2 (64%) above the preinfusion level, stroke volume index rose by 12 ml X m-2 (35%) and heart rate rose by 16 beats X min-1 (20%). There was a significant fall in systemic vascular resistance of 50% manifested by a reduction of 22 mm Hg in systolic blood pressure (18%) and 18 mm Hg in diastolic blood pressure (22%). Pulmonary vascular resistance fell by 45%. Mean pulmonary artery pressure and capillary wedge pressure did not change significantly. This study suggests that concomitant mild to moderate left ventricular failure is not a contra-indication to nicardipine therapy in patients with angina.
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PMID:The acute haemodynamic effects of nicardipine in patients with chronic left ventricular failure. 374 13

A 40-year-old man was admitted to the hospital with pulmonary edema without signs of left ventricular failure. Noncardiogenic pulmonary edema was diagnosed, and a subsequent workup identified a pheochromocytoma as the cause of this condition. The clinical picture could be mimicked by infusion of exogenous norepinephrine. It is concluded that surges of catecholamines from a pheochromocytoma may provoke pulmonary edema in a manner similar to that by which neurogenic pulmonary edema related to cerebral disorders occurs.
Hypertension 1986 Sep
PMID:Noncardiogenic pulmonary edema as the sole manifestation of pheochromocytoma. 374 72

In two children with the haemolytic uraemic syndrome dilated cardiomyopathy occurred in the absence of hypertension, or fluid or electrolyte disturbance. These cases presented with acute left ventricular failure. Echocardiography showed left ventricular dilatation and reduced contractility. There was also ventricular wall thickening, which persisted. Twelve other children with haemolytic uraemic syndrome had prospective echocardiography. Eleven of them showed no evidence of cardiomyopathy and in one transient dilatation and reduced contractility developed without clinical signs. Dilated cardiomyopathy is a rare but important extrarenal manifestation of the haemolytic uraemic syndrome and is best demonstrated by echocardiography.
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PMID:Dilated cardiomyopathy associated with haemolytic uraemic syndrome. 381 52

Systemic and pulmonary hemodynamics have been studied during the induction of brain death in the chacma baboon. In 11 animals brain death was induced by acute intracranial hypertension. Continuous recording of blood flow through both the pulmonary artery and the aorta was obtained by electromagnetic flow meters placed around these vessels. Mean arterial, central venous, pulmonary arterial, and left atrial pressures were recorded continuously. Systemic and pulmonary vascular resistances were calculated. During the agonal period marked sympathetic activity occurred, with significant increases in circulating catecholamines and systemic vascular resistance. The great increase in systemic resistance resulted in acute left ventricular failure. Mean left atrial or pulmonary capillary wedge pressure rose above the mean pulmonary arterial pressure in 9 animals. As the systemic vascular resistance rose, a significant difference between pulmonary artery and aortic blood flows occurred, leading to blood pooling within the lungs. A mean of 72% of the total blood volume of the animal accumulated within these organs. The increase of left atrial pressure to levels higher than pulmonary artery pressure indicated a state of pulmonary capillary blood flow arrest. This, associated with the blood pooling within the lungs, almost certainly resulted in disruption of the anatomic integrity of the pulmonary capillaries (blast injury); 4 animals developed pulmonary edema, with alveolar septal interstitial hemorrhage.
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PMID:Pathophysiology of pulmonary edema following experimental brain death in the chacma baboon. 382 73

Diuretics are the mainstay of drug therapy in the treatment of many cardiovascular disorders. However, perusal of knowledge of their haemodynamic activities in heart failure and hypertension reveals major gaps. In left ventricular failure complicating acute myocardial infarction, intravenous frusemide reduces the elevated left heart filling pressure with little change in systemic blood pressure, heart rate or cardiac output, and restores the ability of the left heart to handle an acute increase in filling volume. But there is little knowledge of the haemodynamic effects of other intravenous diuretics, oral diuretics or diuretics other than those acting on the loop of Henle in this emergency clinical situation. Even less information is available on the haemodynamic effects of diuretics in patients in chronic heart failure. In patients with valvular heart disease, parenteral mercury and oral thiazides reduce right heart and pulmonary vascular pressures with variable (dose-dependent?) changes in cardiac output. Information on the effect of loop diuretics, the comparative effects of intravenous versus oral routes of administration and dose-response correlations are all lacking. In hypertension, the dose-blood pressure lowering response relationship of orally administered diuretics is relatively flat. The majority of information relates to oral thiazides; there is little reliable information on the anti-hypertensive efficacy of the loop diuretics. The acute and chronic effects of the majority of commonly used diuretics on cardiac and peripheral vascular functions is unexplained. More is known of their potentially adverse metabolic effects than of their possible circulatory benefits in hypertensive patients. Many unwanted side-effects of these drugs have been described; their potential importance is related directly to the disease state and doses in which they are used. In acute heart failure, their potential danger is probably minimal. In the treatment of chronic heart failure their most sinister potential is in the excessive secretion of potassium and magnesium. In hypertensive patients their long-term administration in high-doses may lead to undesirable metabolic effects that tend to offset their blood pressure lowering activity. Despite their drawbacks, diuretics continue to provide the natural first-line treatment of choice of these common cardiovascular syndromes. But more information on their mechanisms of vascular activities and the differences in non-diuretic activity between different compounds is urgently required.
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PMID:Diuretics in cardiovascular therapy. Perusing the past, practising in the present, preparing for the future. 389 Mar 92

Theophylline is a widely used bronchodilator, but only recently have its positive cardiovascular actions been recognized in patients with chronic obstructive pulmonary disease (COPD). Intravenous aminophylline acutely reduces pulmonary artery pressures and pulmonary vascular resistance and increases both right and left ventricular ejection fraction. Oral long-acting theophylline produces a similar and chronic improvement in biventricular performance. Postulated mechanisms by which theophylline enhances right and left ventricular systolic pump performance include reduction in ventricular afterload and positive effects of the drug on ventricular inotropy. Theophylline may be particularly valuable in patients with a combination of COPD, pulmonary artery hypertension, and right or left heart failure.
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PMID:Effects of theophylline on cardiovascular performance in chronic obstructive pulmonary disease. 389 23


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