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

The electrical effect of ventricular hypertrophy is evaluated with an idealized model. Perfectly symmetrical hypertrophy is expected to enlarge the QRS complex with a certain proportion of the amplitude and duration. If the conduction velocity is unaltered, the QRS area will be increased proportionally to the myocardial mass. 2) Based on the preservation of the ventricular gradient, the secondary T change is expressed as a function of the QRS and G vectors. A theoretically interesting parameter, G/QRS ratio, is defined as a measure of the "ventricular gradient density," which is important for the over-all recovery pattern. This ratio is decreased in ventricular hypertrophy and is closely related to the QRS-T angle. 3) From the viewpoint of the theory, clinical cases with left ventricular hypertrophy are examined. The theory describes the cases with uncompicated hypertension fairly well, although variations from case to case are not small. Underlying assumptions and causes of deviations in actual cases are discussed.
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PMID:Theoretical considerations on the electrocardiogram of ventricular hypertrophy. 13 Nov 72

The prognosis in chronic myocardial disease is not well defined, partly because of a wide spectrum of clinical courses, and partly because of relatively short observation periods. This paper describes 106 patients followed for 2-12 years. Development or worsening of symptoms after intercurrent infections was associated with a more severe outlook than an insidious debut. The ability to develop myocardial hypertrophy appeared to be an important factor in deciding the prognosis. Pump failure was the cause of death in 80% of the patients, while 16% died suddenly. A favourable course was often noted in patients with ECG signs of left ventricular hypertrophy. This was also the case in patients who developed systemic hypertension. The presence of low voltage, especially in combination with left atrial enlargement, was associated with a malignant development.
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PMID:Chronic myocardial disease. I. Clinical picture related to long-term prognosis. 13 89

The prevalence of signs of heart involvement was studied non-invasively in a group of untreated hypertensives (n=35) and a reference group (n=73), all derived from a random population sample of 50-year-old men. Signs of left ventricular hypertrophy were studied by means of orthogonal electrocardiography and conventional electrocardiography. Signs of decreased distensibility of the left ventricle were studied by apex cardiography and registration of atrial sounds. Left ventricular hypertrophy among hypertensives was significantly more common according to orthogonal electrocardiography (33%) than according to conventional electrocardiography (9%), indicating that the former may be a better method for detection of left ventricular hypertrophy than the latter. In the hypertension group the amplitude of the R wave in lead X on orthogonal electrocardiography was positively correlated to casual diastolic blood pressure (r=0-40) and to diastolic blood pressure after one hour's rest (r=0-65). The degree of pressure load leading to left ventricular hypertrophy seems to be better reflected by resting than by casual blood pressure. There was no hypertensive subject with both signs of left ventricular hypertrophy on orthogonal electrocardiography and either an a/H ratio over 15 per cent or an abnormal atrial sound, indicating two different forms of cardiac involvement as the result of hypertension. Casual blood pressures became normal during rest in hypertensives with a/H ratio over 15 per cent on apex cardiography or abnormal atrial sound, not in hypertensives with signs of left ventricular hypertrophy on orthogonal electrocardiography.
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PMID:Orthogonal electrocardiogram, apex cardiogram, and atrial sound in normotensive and hypertensive 50-year-old men. 13 71

Changes in the density and distribution of pulmonary mast cells were determined in six mammalian species exposed to hypobaric hypoxia (PB = 435 Torr) for 19-48 days. Control animals were studied at 1,600 m (PB = 635 Torr). Total lung mast cell hyperplasia was observed only in calves exposed to high altitude. Pigs, rats, and sheep exhibited small, but insignificant, increases in mast cell density. Perivascular mast cell proliferation adjacent to vessels of 30-500 mum in diameter was seen in both calves and pigs. Bronchial, alveolar septal, and systemic tissue (tongue) mast cell hyperplasia was not observed in any of the species. Three indices of pulmonary hypertension (right ventricular hypertrophy, medial thickness of pulmonary arteries, and pulmonary arterial pressure) correlated with perivascular mast cell density. The findings indicate that perivascular mast cell proliferation may relate more to the morphological pulmonary vascular changes and to pulmonary hypertension than to hypoxia, leading to the speculation that mast cells increase in number in response to the hypertension, rather than to mediate and maintain the hypertension.
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PMID:Lung mast cell density and distribution in chronically hypoxic animals. 13 66

Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypertrophy or dilatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosis or hypertension, or whether it is assymmetrical, which is characteristic of hypertrophic cardiomyopathy. Similarly, dilatation of the heart may be due to volume overload of the left ventricle secondary to valvular insufficiency, congestive cardiomyopathy or ischemic heart disease; these can be distinguished by echocardiography. As certain types of mitral insufficiency are associated with specific valvular dysfunction, the possible etiology of the mitral insufficiency and therefore of the volume overload of the left ventricle may be determined using echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the "large heart."
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PMID:Echocardiography in the differential diagnosis of the large heart. 13 5

The effects of peripheral sympathectomy with nerve growth factor antiserum (NGFAS) on blood pressure, systemic hemodynamics, myocardial function, myocardial hypertrophy, and renin were studied in male spontaneously hypertensive (SH) rats of the Okamoto strain and normotensive control Kyoto-Wistar (WKY) rats. NGFAS prevented the developing of hypertension in the SH rats but did not alter blood pressure in the WKY rats. The NGFAS-treated SH rats developed the same hemodynamic abnormalities as the sham-treated rats, including increased peripheral vascular resistance and depressed cardiac output; Indices of left ventricular performance, including peak flow velocity, stroke power, stroke work, dP/dtmax, and flow acceleration (dF/dt), were diminished in the SH rats compared to the WKY rats. NGFAS treatment further depressed ventricular function in the SH rats, but had little effect on the WKY rats; Plasma renin activity in both the SH and WKY rats was unaffected by NGFAS treatment. Although NGFAS treatment effectively prevented the development of hypertension in the SH rats, it did not influence the development of left ventricular hypertrophy as reflected by increases in left ventricular mass, RNA, DNA, and hydroxyproline content. The data suggest that the development of myocardial hypertrophy and myocardial dysfunction in the SH rat is in part independent of hypertension and plasma renin activity.
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PMID:Development of left ventricular hypertrophy in young spontaneously hypertensive rats after peripheral sympathectomy. 13 13

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

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.
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PMID:Cardiac size and function in acromegaly. 14 34

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.
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PMID:Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension. 14 28

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36


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