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

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.
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PMID:Angina pectoris. Diagnosis and treatment. 0 83

In 25 patients undergoing coronary artery bypass grafting hemodynamic measurements (including values obtained with Swan-Ganz catheterization in 21 of the patients) were made before and after administering a bolus injection of 64 or 96 mcg of nitroglycerin to relieve intraoperative hypertension. This pharmacological agent reduced afterload and preload without raising heart rate. The effect was apparent within 1-3 min and lasted 5-10 min. Untoward hypotension was not encountered in any instance. This intervention appears to be a safe approach to the treatment of intraoperative hypertension in patients with coronary artery disease.
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PMID:Incremental intravenous nitroglycerin for control of afterload during anesthesia in patients undergoing myocardial revascularization. 9 4

To palliate certain criticisms levelled at workers studying psychological factors in coronary artery disease, the authors have applied a pluri-dimensional approach associating a semi-direct psychological interview, a self-evaluation test (Bortner scale), an Eysenck personality test and Sandler and Hazari's test of obsessional behaviour. This protocol was applied to 222 patients hospitalised for coronary artery disease and 522 random controls. The psychological interview and Bortner test showed a significantly higher proportion of A pattern and especially extreme A pattern behaviour in patients with coronary artery disease (32.6 % in coronary patients 9.7 % in controls). The personality questionnaire showed a greater tendency to neurotic behaviour in the coronary patients. These results were independant of age and sex. In the present study, psychological factors are given equal importance to other major risk factors (tobacco, hypertension, hypercholesterolaemia). They are independant of these other factors. A prospective study using the same protocol is being prepared.
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PMID:[Pluri-dimensional study of psychological factors in coronary disease]. 10 94

A group of ten acromegalic patients, who had no history of heart failure, was studied to determine whether subtle carciac impairment may also be common. None had clinical evidence of coronary artery disease or severe hypertension. Systolic time intervals were recorded in each patient and compared with normal values predicted for sex and heart rate by our own controls and published data. The results indicate that measurable abnormalities in left ventricular performance are common in this sampling. Known duration and activity of disease (growth hormone levels at time of study) did not correlate with the time intervals. The results are consistent with cardiomyopathic effect of excessive growth hormone.
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PMID:Evidence of subclinical heart muscle dysfunction in acromegaly. 12 91

The clinical, hemodynamic, and angiographic findings were correlated with the heart size in 207 patients with proved coronary artery disease. Cardiomegaly was noted in 34 patients and normal heart size in 173. In these two groups, the patients' age range, duration of disease, and history of myocardial infarction were similar. There was no statistical difference in incidence of shortness of breath, hypertension, left ventricular hypertrophy, or abnormal glucose tolerance. Patients with cardiomegaly had a significantly higher incidence of congestive heart failure (26 per cent) as compared to patients with normal heart size (2.9 per cent) (P less than 0.001). Patients with enlarged heart presented a high incidence of anterior wall or multiple myocardial infarction (73 per cent) (P less than 0.001). The cardiomegaly group had a high incidence of elevated end-diastolic volumes, elevated end-diastolic pressures, and diminished ejection fractions when compared to patients with normal heart size (P less than 0.01). Double and triple coronary artery disease was more frequent in patients with cardiomegaly and total coronary score was also higher in this group (P less than 0.005). Asynergy was present in 55 per cent of patients with normal heart size but in 82 per cent of those with enlarged hearts (P less than 0.01). The group of patients with cardiomegaly and documented congestive heart failure had ejection fractions less than 0.30. Cardiac catheterization is probably not advisable in these patients in the absence of associated significant mitral regurgitation, ventricular septal defect, or ventricular aneurysm.
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PMID:Correlation of heart size with clinical and hemodynamic findings in patients with coronary artery disease. 12 83

Mitral reguritation is a relatively common finding in coronary heart disease. In this series of 127 patients, selected with a view to coronary or left ventricular surgery on the basis of severity of symptoms, the incidence was 39 (31%). Mitral regurgitation is significantly more common in patients with a history or electrocardiographic evidence of previous myocardial infarction. Clinically it may present as a pan- or late systolic or even a mid-systolic, ejection type murmur at the apex or at the left sternal edge; but in 39 per cent of the patients with angiographic mitral regurgitation no murmur was present. Angiographically important mitral regurgitation (grades 2-4/4) was usually associated with a systolic murmur; this finding was independent of ejection fractions. Left ventricular enlargement clinically or radiographically is likely to accompany mitral regurgitation but left atrial enlargement (electrocardiographically or on chest x-ray) is a more reliable pointer to mitral regurgitation and pulmonary venous hypertension is even more strongly suggestive of its presence. The electrocardiographic signs of papillary muscle infarction were rare in this series (15%) and were not related to angiographic mitral regurgitation. There was no difference in the incidence of mitral regurgitation in association with anterior or inferior myocardial infarction or in distribution of coronary artery disease. There is, however, a higher incidence of mitral regurgitation in more severe coronary arterial disease (P less than 0-05). The incidence of mitral regurgitation is significantly higher with reduction in left ventricular ejection fraction (P less than 0-001), with rise in the left ventricular end-diastolic pressure (P less than 0-02), and with abnormal contraction patterns, but the severity of mitral regurgitation is not significantly related to these findings.
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PMID:Mitral regurgitation in coronary heart disease. 13 31

The data regarding the effect of physical of physical conditioning on the progression of myocardial is chemia, although suggestive of a favorable influence, are in no way definitive. Efforts to alter the physical activity habits of our population should not supersede efforts directed to alter the major risk factors. The emphasis in the prevention of coronary atherosclerotic heart disease for the general public should be on the well established cardinal risk factors, that is, hypercholesterolemia, hypertension, and cigarette smoking. The National Postinfarction Rehabilitation Study, when completed, may demonstrate how physical conditioning influences the progression of myocardial ischemia. However, "moderate activity is a part of a balanced satisfying living and is the safe and sane hygienic prescription of the thoughtful physician for his patients, the high risk and the healthy alike.
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PMID:Does exercise conditioning delay progression of myocardial ischemia in coronary atherosclerotic heart disease? 13 6

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.
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PMID:Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta. 14 28

Assessment of the pathophysiologic changes associated with systemic hypertension has been limited by difficulty in justifying invasive studies of the left ventricle. Echocardiography, because it is notinvasive, offers an attractive method of assessing cardiac dimensions and function in hypertensive heart disease. Fourteen age-matched normotensive subjects and 31 patients with hypertension (but without clinical evidence of coronary artery disease) were studied before receiving any antihypertensive therapy. The patients with hypertension were classified into three groups on the basis of previously established electrocardiographic and chest X-ray criteria: group I, normal electrocardiogram and chest roentgenogram (13 patients); group II, left atrial abnormality by electrocardiogram and a normal chest roentgenogram (8 patients); and group III, left ventricular hypertrophy by electrocardiogram or chest roentgenogram, or both (10 patients). Mean arterial pressure increased significantly from group I to group II and from group II to group III (P is less than 0.01), and this increase was associated with a similar progressive increase in left ventricular mass assessed with echocardiogram (P is less than 0.01). A significant increase was also found in both posterior wall and septal thickness in groups II (P is less than 0.05) and III (P is less than 0.01). In association with this increased mass a significant decrease in ejection fraction and fractional fiber shortening was demonstrated in groups II (P is less than 0.05) and III (P is less than 0.01) although cardiac index was reduced only in group III (P is less than 0.05). Thus, increased ventricular mass can be identified with echocardiography at an early stage of hypertensive heart disease when only left atrial abnormality is identifiable with electrocardiographic criteria and decreased left ventricular performance occurs with increasing arterial pressure and left ventricular hypertrophy.
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PMID:Pathophysiologic assessment of hypertensive heart disease with echocardiography. 14 Jun 1

The aim of this study was to compare the ability of electro- and echocardiography to detect enlargement of the left atrium. Seventy-four patients, divided into three groups (eighteen normal, thirty-six valvular disease, twenty hypertension and/or coronary artery disease) were studied. The P wave terminal force in lead V1 (PTF-V1) was measured from a standard 12 lead electrocardiogram, and the internal left atrial dimension (LAD) was measured from time-motion echocardiograms. Linear regression analysis showed a small but significant linear correlation between PTF-V1 and LAD (r = 0-32, P less than 0-01). Both methods would separate patients with diseases known to cause left atrial enlargement from normals, but echocardiography showed greater "specificity" (100% v. 94+) and "sensitivity" (75% v. 67%). It was much superior to the ECG in detecting milder grades of left atrial enlargement and for following serial changes.
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PMID:The non-invasive recognition of left atrial enlargement: comparison of electro- and echocardiographic measurements. 14 46


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