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

Optimal care of the patient with heart disease undergoing noncardiac surgery requires that the members of the surgical team, including anesthesiologist, internist-cardiologist, and surgeon, be familiar with the cardiovascular response to surgery, preoperative cardiac risk stratification, and the unique pathogenesis of cardiac complications that may occur in the perioperative period. Preoperative evaluation and computation of cardiac risk, anesthetic considerations, along with perioperative care of the patient with ischemic heart disease, valvular heart disease, congestive heart failure, arrhythmias and conduction disorders, and hypertension is discussed.
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PMID:Noncardiac surgery in the patient with heart disease. 355 69

In the International Prospective Primary Prevention Study in Hypertension, electrocardiographic changes before and during 3- to 5-year antihypertensive treatment were investigated in a cohort of 5819 men and women aged 40 to 64 years with entry diastolic blood pressures of 100 to 125 mm Hg. They were randomly allocated to treatment regimens that either included or excluded the slow-release beta-blocker oxprenolol. Electrocardiograms (ECGs) were assessed using the Minnesota Code and assigned to groups of normal ECGs or ECGs with pressure-related, ischemic, "intermediate," or "other" abnormalities. Antihypertensive treatment was associated with a decrease (mainly in men) of pressure-related and (mainly in women) of intermediate abnormalities. Ischemic abnormalities increased, particularly in men. Inclusion of the beta-blocker resulted in a greater reduction in intermediate abnormalities and in a lesser increase in ischemic abnormalities. Better blood pressure control was associated with a lesser increase in ischemic abnormalities and in a regression of pressure-related abnormalities. The presence of ST segment depression and of a complete left bundle branch block in the entry ECG was associated with a significant risk for sudden death and myocardial infarction. Optimal blood pressure control prevents pressure-induced cardiac target organ damage and, hence, heart failure, and may delay the progression of ischemic abnormalities. This tallies with the lower critical cardiac event rate associated with lower blood pressure that was observed in the same study.
Hypertension 1987 Jun
PMID:Electrocardiographic changes during antihypertensive therapy in the International Prospective Primary Prevention Study in Hypertension. 359 89

Elevated blood pressure is a major contributor to cardiovascular disease in general and to coronary heart disease in particular, now its most common sequela. The risk is proportional to the degree of blood pressure elevation, at all ages and in either sex, whether the increased pressure is labile or fixed, diastolic or systolic in character. The effect of blood pressure on cardiovascular disease incidence is independent of the influence of other predisposing co-factors, but the hazard is greatly influenced by them. Elevated pressures are often accompanied by hyperlipidaemia, hyperuricaemia, overweight, hyperglycaemia, elevated fibrinogen values and ECG abnormalities. The risk associated with any degree of elevation of pressure varies greatly, depending on the number and level of these often associated risk factors, and on whether or not there is the indication of target organ involvement. The excess cardiovascular risk in hypertensive persons tends to be concentrated in those with an increased LDL/HDL cholesterol ratio, impaired glucose tolerance, cigarette smokers and those with accompanying ECG abnormalities. Hypertension is best conceptualised as a component of a multivariate cardiovascular risk profile which provides a sound basis for determining urgency for drug treatment. Optimal preventive management of hypertension requires multifactorial correction of all disordered components of the cardiovascular risk profile before occurrence of target organ involvement.
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PMID:Hypertension. Relationship with other risk factors. 372 May 67

Contributors to CHD include atherogenic personal attributes, living habits which promote these, signs of preclinical disease, and host susceptibility to these influences. Atherogenic traits include the blood lipids, blood pressure, and glucose tolerance. High LDL cholesterol is positively and high HDL cholesterol inversely related to CHD incidence. Hypertension, whether systolic or diastolic, labile or fixed, casual or basal, at any age in either sex contributes powerfully to coronary heart disease. The impact of diabetes on CHD is greater for women than for men and varies according to the level of the foregoing risk factors. The faulty life-style is typified by a diet excessive in calories, fat, and salt, a sedentary habit, unrestrained weight gain, and cigarettes. Alcohol used in moderation may be beneficial. Oral contraceptives worsen atherogenic traits and, when used for long periods beyond age 35 in conjunction with cigarettes, predispose to thromboembolism. Type A persons with an overdeveloped sense of time urgency, drive, and competitiveness develop an excess of angina pectoris. Men married to more highly educated women are at increased risk, as are men married to women in white-collar jobs. Preclinical signs of a compromised coronary circulation include silent MI, ECG-LVH, blocked intraventricular conduction, and repolarization abnormalities. Exercise ECG may elicit still earlier evidence. Measures of innate susceptibility include a family history of premature cardiovascular disease, diabetes, hypertension, and gout. Optimal prediction of CHD requires a quantitative combination of risk factors in multiple logistic risk formulations that identify high-risk persons with multiple marginal abnormalities. Preventive management should also be multifactorial.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Psychosocial and other features of coronary heart disease: insights from the Framingham Study. 377 1

Early reports on SLE were too small in number to determine that pregnancy was contraindicated in patients with renal involvement. Later reports show that patients with lupus nephropathy can have successful pregnancies provided certain preconditions are established. Optimal preconditions include prepregnancy remission of at least 6 months, renal function with serum creatinine 1.5 mg/dl or less or creatinine clearance of 60 ml/min or more or proteinuria of 3 g/24 hr or less. Successful pregnancies have been recorded in some patients with more severe renal impairment. Renal function will remain unchanged in approximately 60% of pregnancies; and although deterioration may occur, it is only severe or permanent in less than 10%. In 26% of patients, mild to severe renal impairment was transient, with recovery to prepregnancy levels of renal function. Proteinuria with good creatinine clearance may not be dangerous. Hypertension or superimposed preeclampsia jeopardizes the outcome. Fetal outcome averaged approximately 70% (range, 41-77%) live births, 17.8% (range, 5.1-40%) spontaneous abortions, 19.7% (range, 3.0-38.5%) prematurity, and 8.2% SGA. Therapeutic abortion is not a modality of treatment of lupus nephropathy. Management of patients with lupus nephropathy is twofold and includes suppression of underlying lupus activity as well as the serial evaluation of chronic renal disease. In chronic lupus nephropathy with inactive SLE maternal and fetal outcome is the same as for pregnant patients with chronic renal disease of other causes. Strict fetal surveillance must be performed to decrease the stillbirth rate. The concomitant increase in prematurity demands the services of a tertiary care neonatal unit. Management necessitates the team approach of the obstetrician, nephrologist, rheumatologist, and neonatologist working in collaboration. The reports which contain large numbers of patients now allow better counseling of these patients who are contemplating pregnancy.
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PMID:Lupus nephropathy and pregnancy. 389 19

Forty-six patients who underwent renal artery repair for presumptive renovascular hypertension are presented. Preoperative investigation included a rapid sequence IVP, a high quality angiogram and split function studies, as well as renin assays of renal venous blood in the more recent cases. Atherosclerosis was the causative pathological lesion in 60% of the patients, with fibromuscular dysplasia or miscellaneous causes of stenosis accounting for the remaining 40%.Surgical correction was usually obtained by bypass grafting (57%). Hypertension was cured or significantly improved in 36 patients (78%).Optimal results are dependent upon complete preoperative investigation and surgical repair of all the stenotic areas.
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PMID:Reconstructive vascular surgery for renovascular hypertension. 459 Jul 96

CBA mice develop hypertension when placed in complex population cages that facilitate social interactions and competition for territory. After 1 month, these mice have normal plasma renin levels, but blockade of converting enzyme lowers blood pressure to normal. To test the possibility that this normal-renin hypertension is caused by enhanced pressor responsiveness to angiotensin II (AII), we examined the effects of AII on hindquarter and renal vasculatures from 13 hypertensive and 13 normotensive mice. Both vascular beds were pump-perfused at a constant flow with plasma substitute. Optimal perfusion flows and basal pressures were similar in hindquarter (8 ml/100 g/min; 60 mm Hg) and renal vasculatures (130 ml/100 g/min; 50 mm Hg) from normotensive and hypertensive mice. Threshold constrictor responses to AII were elicited at a significantly lower dose in both vasculatures of hypertensive mice than in those of normotensive mice. Maximal pressor responses to AII were greater in the hindquarters of hypertensive mice than in those of normotensive mice, but were not different in the renal vasculatures of the two groups. Vasoconstrictor sensitivity to norepinephrine was also increased in the hindquarters of hypertensive mice; however, the changes in threshold and maximal pressor response were less than for AII. Responsiveness to norepinephrine in the renal vasculatures of hypertensive mice was not different from that in the kidneys of normotensive mice. We conclude that the hyperresponsiveness to AII in the resistance vessels plays an important role in maintaining elevated blood pressure in this psychosocial model of hypertension.
Hypertension
PMID:Increased vascular sensitivity to angiotensin ii in psychosocial hypertensive mice. 682 25

Women with severe pregnancy-induced hypertension are often critically ill; their fetuses are usually compromised. An ideal anesthetic method does not exist for the parturient with severe hypertension, hypovolemia, and organ failure. Optimal anesthetic results depend upon thorough preanesthetic evaluation and best medical control of pathophysiology, regardless of the technique employed for vaginal or cesarean delivery. The anesthesia team must be consulted early, communicate freely and effectively with other perinatal team members, and have extensive knowledge of the pathophysiology involved. Time must be allowed for preparation of necessary monitoring and anesthetic facilities. In patients under good medical control, judiciously administered continuous epidural block is the better approach for labor, vaginal delivery, or cesarean section.
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PMID:Anesthesia for pregnancy-induced hypertension. 706 27

Combined use of prazosin and propranolol was effective in preoperative management of three patients with norepinephrine(NE)-secreting pheochromocytoma (PHEO). On admission, all were symptomatic and had moderate to severe hypertension despite treatment with diuretics, propranolol, and sympatholytics. Optimal symptomatic and blood pressure (BP) control was achieved with 6 to 10 mg/day prazosin and 120 to 480 mg/day propranolol every 6 hr in equally divided doses. With this therapy, BP and hematocrit were reduced to levels similar to those found in the postoperative period. The daily urinary excretion of catecholamines and their metabolites was not modified during therapy with prazosin and propranolol. There was a drop in supine systolic (40 to 64 mm Hg) and diastolic (32 to 52 mm Hg) BP in all patients 1 to 2 hr after the first dose of prazosin (1-mg tablet); in two subjects this was accompanied by a larger orthostatic fall (74 and 92 mm Hg systolic; 65 and 78 mm Hg diastolic BP). The high incidence of first-dose effect suggests that a single oral dose of 1 mg of prazosin could aid in the diagnosis of PHEO. The effectiveness of prazosin in controlling the hypertension induced by NE-secreting PHEO suggests that, in man, pressure responses to augmented levels of NE are mediated solely through alpha 1-receptors.
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PMID:Prazosin and propranolol in preoperative management of pheochromocytoma. 709 3

Prognosis of heart transplant patients has dramatically improved in the last decade thanks to the use of cyclosporine as immunosuppressive treatment. Optimal follow-up and early recognition of complications and side effects of treatment lead to longer survival and marked improvement of these patients' quality of life. However, the incidence of complications remains high and their management calls for particular care. We review our experience of heart transplantation in Lausanne and describe in detail the results and complications such as rejection, transplant coronary artery disease, hypertension, renal failure, metabolic disorders, cancer and conduction problems. Cooperation of the medical team (cardiologist, surgeon, anesthetist, general practitioner) is essential to long term success of the transplant program.
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PMID:[Patient management following cardiac transplantation]. 748 49


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