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

The prevention of cardiovascular disease antedates our current preoccupation with risk factors for coronary heart disease and hypertension. Indeed, earlier preventive efforts have in part been so successful that many people have forgotten that they existed. The almost forgotten entity, beriberi heart disease, was first prevented in 1883 by Takaki of Japan. With diphtheria, it was the identification of the causative bacillus by Klebs in 1883, leading finally to the development of diphtheria toxoid by Ramon in 1923, which resulted in the disappearance of diphtheritic heart disease. Success in the attack on syphilitic heart and vascular disease began with Bordet and Gengou in 1901 with the discovery of the phenomenon of complement fixation, and with the formulation of Salvarsan by Ehrlich in 1907. The story of the prevention of rheumatic fever has a large cast of characters, but special recognition must be given to Coburn for his observations confirming the role of the hemolytic streptococcus published in 1931 and showing the prophylactic value of sulfanilamide published in 1939. The important association of maternal rubella with congenital heart malformations was revealed by Gregg in 1941. Alcoholic heart disease was identified particularly by Brigden and Evans in 1957 and 1959, respectively. In relation to coronary and hypertensive heart disease, the names of Anitschkow (1933), Leary (1935), and Keys (1948) in relation to diet, of Freis (1967) in the field of hypertension treatment, of White (1927) in relation to physical exercise, and of English, Willius, and Berkson (1940) and Hammond and Horn (1954) in the role of cigarette smoking, deserve special recognition.
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PMID:Background of the prevention of cardiovascular disease. II. Arteriosclerosis, hypertension, and selected risk factors. 266 Oct 54

To study the earliest changes in left ventricular structure and function appearing in response to hypertensive heart disease the study was started with an initial group of subjects detected for the first time in their lives with elevated levels of systemic blood pressures. A careful follow up of these subjects during the next year allowed the division of these subjects into a group of healthy not hypertensive subjects and a group of subjects with mild essential systemic hypertension detected in an early phase. The next six years of repeated controls (arterial blood pressure measurement, clinical examination, routine chest X-ray pictures, standard 12 leads ECG and M-mode echocardiography) allowed a further division of the hypertensive subjects into two groups of patients: one correctly treated and the other treated incorrectly or not at all. It was found that left ventricular diastolic functions expressed by left ventricular relaxation time index (LVRTI) and left atrial emptying index (LAEI) are the earliest indicators of hypertensive heart disease due to mild essential systemic hypertension.
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PMID:Left ventricular relaxation time index and left atrial emptying index as early echocardiographic indicators in predicting hypertensive heart disease. 274 54

Hypertensive heart disease has an important place among the cardiovascular diseases. There are evidences that the behavior of arterial tension (AT) in children can predict the possible appearance of arterial hypertension (AH) in the adult. The foreign percentile curves, when applied to our population, show either under or overestimation of the cases. This is the reason for the need of having our own percentile tables. In this study we found different mean values for systolic and diastolic arterial tension (SAT and DAT) between the sexes, being these higher for the males, but these differences had no statistical significance. We present percentile tables for AT per sex against age, weight, height and corpulence index (CI). According to WHO, when a child has three measurement over the 95 percentile he should be considered AH. The tables for height, weight, and CI should be used only under special circumstances.
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PMID:[Percentile curves of arterial tension in school children from Mexico City]. 275 38

Epimyocardial excitation is delayed in areas overlying infarcted myocardium. On the assumption that a delayed R peak in V6 could indicate anterior myocardial infarction (AMI) in the absence of diagnostic Q waves, the findings of angiocardiography (n = 148) and thallium scanning (n = 46) of 194 patients with suspected coronary heart disease (CHD) were compared with regard to two criteria: A (R peak in V6 precedes S peak in V2, or both peaks occur simultaneously, n = 158) and B (R peak in V6 is later than S peak in V2 [R peak delay in V6], n = 36). Of 92 patients with unconfirmed CHD, 4 fit criterion B, and 3 of these had hypertensive heart disease. In 102 patients with confirmed CHD, B was present in 15 of 79 evaluated with angiocardiography and in 17 of 23 patients who had nuclear scanning. Anterior akinesis or dyskinesis was more prevalent in group B (13 cases, 86%) than in group A (17 cases, 26.6%; p = 0.000), as were irreversible anterior thallium defects, with 16 cases in group B (94.1% and 3 cases in group A (50%) (p = 0.016). Two of the three false positives had anterior hypokinesis and one had hypertensive cardiovascular disease. B was less sensitive (59.2%) but demonstrated a specificity of 95.2% and a positive predictive value of 80.6% for the detection of AMI. If used in conjunction with C (poor or reverse R wave progression from V1 to V4, notching at the R upstroke or rsR' in V4, V5, or V6), sensitivity was decreased (38.6%) but false positives were eliminated (specificity and positive predictive value reached 100%). Thus, in the setting of CHD, B can be recommended as a marker of non-Q wave AMI, and its diagnostic reliability is maintained, even in systemic arterial hypertension, if C is taken into consideration.
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PMID:R peak delay in V6. Diagnostic implications in coronary heart disease. 279 37

Hypertrophy in response to increasing blood pressure in primary hypertension leads to important functional consequences for the left ventricle. In fact, the progression of hypertensive heart disease, from an adaptive left ventricular hypertrophy with compensated ventricular function to severe hypertrophy with left ventricular failure, has been long thought to be related to the severity and duration of hypertension. Antihypertensive treatment seems to prevent or minimize the occurrence of left ventricular hypertrophy, but questions arise as to whether this therapy is also able to restore normal hemodynamic conditions, or at least to minimize the hemodynamic abnormalities. This review aims at summarizing current knowledge on the effects of the antihypertensive treatment with beta-blockers, including tertatolol, on hypertension-induced left ventricular hypertrophy. The pathogenetic mechanisms underlying the cardiovascular changes associated with hypertension are discussed. A decrease in left ventricular wall thickness as well as in left ventricular mass has been reported in most of the studies performed with different types of beta-adrenergic blocking agents. The extent of this reduction seems to be related not only to the fall in systemic blood pressure, but also to a decrease in sympathetic stimulation. With regard to the functional consequences of hypertension, the reversal of left ventricular hypertrophy following antihypertensive treatment with beta-blockers is usually associated with an improvement in left ventricular performance. This phenomenon can hardly be ascribed to the direct effects of beta-blocking agents. It is more likely to be related to the concomitant reduction in the afterload and to the improved left ventricular compliance, associated with a decrease in left ventricular wall thickness.
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PMID:Reversal of left ventricular hypertrophy following treatment with beta-blockers: experience with tertatolol. 287 79

The criteria of the degree of hypertrophy and dilatation are defined. On this basis, functional and therapeutical regimen of regression of cardiac hypertrophy (prazosin, clonidine, nifedipine) are analyzed in concentric as well as in excentric hypertrophy in patients with arterial hypertension. Regression of cardiac hypertrophy is possible by differentiated pharmacotherapy, e. g., by prazosin, calciumantagonists, clonidine, alphamethyldopa, ACE-inhibitors as well as by combination therapies (beta-receptor blocking agents plus diuretics plus vasodilators). By these therapeutical measurements improvements in ventricular function can be achieved. Coronary reserve can be improved, consecutively the ischemic risk of hypertrophied cardiac muscle may be reduced. By the availability of pharmacotherapeutical regression of cardiac hypertrophy differentiated pharmacotherapy is possible in cardiac hypertrophy in man. Parallel to the regression improvement in ventricular function is possible. It remains still investigated, whether pharmacotherapeutical regression of cardiac hypertrophy is associated with decrease in coronary and late myocardial complications and whether prognosis of hypertensive heart disease can be significantly improved.
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PMID:[Progression and regression of heart hypertrophy in arterial hypertension: pathophysiology and clinical aspects]. 293 17

Left atrial function in patients with hypertensive heart disease was compared with that in control subjects. In patients with hypertensive heart disease, the time constant of left ventricular relaxation was significantly greater than that in controls (54 +/- 18 vs 31 +/- 16 msec; p less than 0.01). The ratio of left ventricular filling volume before atrial contraction (left atrial reservoir volume/left atrial emptying volume before atrial contraction, and conduit volume/flow volume from the pulmonary vein into the left ventricle) to left ventricular stroke volume was significantly smaller than that in controls (65 +/- 13 vs 76 +/- 7%; p less than 0.05). In patients with hypertensive heart disease, the ratio of reservoir volume to stroke volume was not significantly different from that in controls, while the ratio of conduit volume to stroke volume was significantly smaller than that in controls (43 +/- 13 vs 57 +/- 9%; p less than 0.05). The latter ratio was inversely correlated with the time constant of left ventricular relaxation (r = -0.05, p less than 0.05). In patients with hypertensive heart disease, the ratio of left ventricular filling volume during atrial contraction to stroke volume was significantly larger than that in controls (35 +/- 13 vs 24 +/- 7%; p less than 0.05). The ratio of left ventricular filling volume during atrial contraction to stroke volume had a significant inverse correlation with the ratio of conduit volume to stroke volume (r = -0.84, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Sep
PMID:Assessment of left atrial function in patients with hypertensive heart disease. 294 77

An abnormal electrocardiographic P wave (AEPW) has been interpreted as indicative of heart failure, hypertrophy or dilatation of left atrium, or diminished left ventricular compliance. In order to determine the significance of this electrocardiographic sign we studied 47 cases of systemic arterial hypertension (SAH) without heart failure or coronary obstruction. Patients were assigned at 2 groups: group A (22 cases with P wave duration greater than 0.11 seg. (LEAD D2); and group B 25 cases with P wave duration less than this. The following data were studied in all cases: left ventricular ejection fraction (LVEF), left ventricular presystolic filling fraction (LVPFF), Sokoloff electrocardiographic index (SEI), final diastolic pressure of LV (FDPLV), and systolic arterial pressure (SAP). Results were: (Table: see text). There were not statistical differences in these values between groups A and B (including the FDPLV value not shown in the table). Correlation coefficient between duration of P wave and the other parameters studied were also no significant. AEPW in SAH is not related to an specifically degree of left ventricular hypertrophy or disfunction; therefore, hypertensive heart disease should not be classified taking in account this electrocardiographic sign.
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PMID:[The P-wave in systemic arterial hypertension]. 294 53

A wide variety of approaches to M-mode echocardiographic methods for estimation of left ventricular mass have been proposed and employed in hypertensive heart disease. The cube function geometry, which assumes an ellipsoid of revolution with a length twice the minor axis, appears to be optimal provided left ventricular shape is relatively normal. The Penn measurement technique for wall thickness and diameter is best validated, but American Society of Echocardiography measurements can be used with appropriate regression correction. Changes in instrumentation may warrant reexamination of measurement techniques as well as the relative value of M-mode and two-dimensional echocardiographic techniques for estimation of left ventricular mass.
Hypertension 1987 Feb
PMID:Standardization in the measurement of left ventricular wall mass. M-mode echocardiography. 294 9

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary sinus blood flow (gas chromatic argon technique) was determined in patients with left ventricular hypertrophy, with or without dilatation, associated with entirely normal coronary arteriographic results: 12 patients with hypertrophic obstructive cardiomyopathy (left ventricular mass-to-volume ratio, 3.66 +/- 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (left ventricular mass-to-volume ratio, 2.12 +/- 0.26 g/ml), 18 patients with hypertensive dilatation (left ventricular mass-to-volume ratio, 1.6 +/- 0.48 g/ml), six patients with aortic stenosis (left ventricular mass-to-volume ratio, 1.99 +/- 0.41 g/ml), 12 patients with aortic incompetence, and 20 patients with normal heart function. Coronary sinus blood flow was determined as a control value and as the value following intravenous injection of dipyridamole (0.5 mg/kg of body weight). Coronary reserve was calculated as the ratio of coronary resistance before and after dipyridamole. Normal coronary reserve averaged 4.89 +/- 0.11. Similar values, despite marked left ventricular hypertrophy, were present for both hypertrophic obstructive cardiomyopathy (4.4 +/- 0.19) and aortic stenosis (4.66 +/- 0.12), whereas coronary reserve was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 +/- 0.19) (p less than 0.001). Moderate decrease in coronary reserve was found in aortic incompetence and in dilated essential hypertension. These results indicate that patients with nonhypertensive hypertrophy, despite left ventricular mass augmentation, may have normal coronary reserve, whereas at a comparable degree of left ventricular hypertrophy, patients with hypertensive hypertrophy have a specific reduction in coronary reserve. Independent from vascular effects, ventricular dilatation may result in deterioration of coronary reserve because of an abnormal component of coronary vascular resistance. These results were also verified in experimental hypertension. Moreover, prevention and/or regression of the impaired coronary circulation in experimental hypertensive heart disease, most probably due to the reduction of smooth muscle layers of the media of coronary resistance vessels, could be achieved by long-term vasodilator therapy.
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PMID:Coronary hemodynamics in hypertensive heart disease. Basic concepts, clinical consequences, and experimental analysis of regression of hypertensive microangiopathy. 297 65


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