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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diastolic wall stress and compliance were determined in 74 patients with essential hypertension during diagnostic cardiac catheterization. Ventricular compliance was normal in compensated essential hypertension without coronary artery disease even at severe left ventricular hypertrophy. In contrast, additional coronary stenosis and ventricular dilatation due to cardiac decompensation was asscociated with considerable decrease in ventricular compliance. Thus, left ventricular hypertrophy in essential hypertension does not imply per se a change in ventricular compliance. A decrease in ventricular compliance was followed by a decrease of forward pump function of the left ventricle. whereas ventricular work index (as estimated as the product out of systolic wall stress and the stroke volume) increased. This disproportion between external and internal ventricular work increased with increasing ventricular dilatation and was greatest in decompensated essential hypertension. Accordingly, decompensated essential hypertension had largest ventricular work load and lowest forward pump function in comparison to all other patient groups with essential hypertension. The mass to volume ratio may be considered an important determinant of the degree of left ventricular hypertrophy in essential hypertension. The relationship between the mass to volume ratio and the systolic wall stress may provide a diagnostic and prognostic evaluation of the left ventricle in essential hypertension on the basis of dynamic ventricular geometry.
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PMID:[The heart in hypertension. III. Determinants of left ventricular hypertrophy and diastolic left ventricular compliance (author's transl)]. 15 7

To investigate the predisposing factors and the clinical significance of the musical aortic component of the second heart sound (musical S2), 18 patients with musical S2 (musical group) among the consecutive 2,000 patients with phonocardiographic examination were noninvasively studied by analyzing underlying diseases, phonocardiographic findings, organic changes of the aortic valve, severity of aortic regurgitation and left ventricular dysfunction. Organic changes of the aortic valve were assessed by two-dimensional echocardiography, and aortic regurgitation was assessed by color Doppler flow imaging. Twenty-two normal subjects (normal group) and 17 patients with essential hypertension (hypertensive group) served as controls. Mean ages were matched among the three groups. 1. Left ventricular dilatation (seven patients) and hypertension (six patients) were the dominant part of underlying disease in the musical group. 2. Musical S2 was classified in the following two types based on the phonocardiographic characteristics; musical vibrations followed immediately after the accentuated S2, and the S2 which was replaced by regular vibratory waves. 3. Frequency of the musical vibrations ranged from 120 to 200 Hz, and its duration ranged from 60 to 120 msec. Amplitude of the musical vibrations decreased by inhalation of amyl nitrite, but increased by infusion of methoxamine. In a case with mild rheumatic valve disease, methoxamine induced marked intensification of the amplitude and prolongation of the duration of the musical vibrations, finally giving a typical cooing murmur. 4. Echo intensity of the aortic valve tended to be higher in the musical group than in the other two groups. 5. Echocardiographically, aortic regurgitation appeared more frequently in the musical group (88%) than in the normal (36%) and hypertensive (41%) groups. Area of the aortic regurgitant signal was significantly larger in the musical group (4.1 +/- 1.4 cm2) than in the normal (1.2 +/- 0.8 cm2) and hypertensive (2.3 +/- 1.2 cm2) groups. 6. Left ventricular end-diastolic dimension was significantly larger in the musical group (5.8 +/- 0.6 cm) than in the normal (4.7 +/- 0.5 cm) and hypertensive (4.8 +/- 0.7 cm) groups. Fractional shortening of the left ventricle was significantly smaller in the musical group (26 +/- 10%) than in the normal (37 +/- 5%) and hypertensive (37 +/- 8%) groups. In a case of the musical group, musical vibrations following the S2, which was large in amplitude at the state of heart failure, decreased markedly after the recovery from heart failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Possible mechanism of production of the musical second heart sound and its clinical significance]. 188 56

This study correlates variables derived from blood pressure (BP) and heart rate (HR) monitoring with the degree of left ventricular structural changes in essential hypertension. Forty patients with mild-to-moderate hypertension according to World Health Organization criteria underwent 24-hour ambulatory monitoring. Echocardiographic (posterior wall and interventricular septum thickness, left ventricular mass) or ECG (SV1 + RV5) indices of hypertrophy were significantly (p less than 0.01) correlated (positive correlations) with derivatives of BP monitoring (mean systolic and diastolic BP values) but not with HR derivatives. Echocardiographic indices of dilatation (left ventricular end-diastolic volume and diameter) were significantly (p less than 0.01 to less than 0.001) correlated (negative correlations) with derivatives of HR monitoring (mean HR values, mainly during the night) but not with BP derivatives. It is concluded that in essential hypertension, left ventricular hypertrophy depends on mean 24-hour systolic and diastolic BP values, whereas left ventricular dilatation appears to be more prominent in patients with bradycardia mainly during the night.
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PMID:Effect of 24-hour blood pressure and heart rate variations on left ventricular hypertrophy and dilatation in essential hypertension. 213 39

Myocardial hypertrophy may influence coronary hemodynamics variably. Therefore, coronary blood flow (CBF) (gas chromatic argon technique) was determined in patients with left ventricular (LV) hypertrophy, with or without dilatation, associated with exclusively normal coronary arteriogram: 12 patients with hypertrophic obstructive cardiomyopathy (HOC) (LV mass to volume (M/V) ratio: 3.66 + 0.52 g/ml), 22 patients with hypertensive heart disease due to essential hypertension (EH) (LV M/V ratio: 2.12 + 0.26 g/ml), 18 patients with hypertensive dilatation (M/V ratio: 1.6 + 0.48 g/ml), 6 patients with aortic stenosis (LV M/V ratio: 1.99 + 0.41 g/ml), 12 patients with aortic incompetence (AI), 20 patients with normal heart function. CBF was determined as (A) controls and (B) following the intravenous injection of dipyridamole (0.5 mg/kg body weight). Coronary reserve (CR) was calculated as the ratio of coronary resistance before and after dipyridamole. Normal CR averaged 4.89 + 0.11 similar values despite marked LV hypertrophy, were present for both HOC (4.4 + 0.19) and as (4.66 + 0.12), whereas CR was considerably reduced in the concentrically hypertrophied hypertensive hearts (3.22 + 0.19) (p less than 0.001). Moderate decrease of CR was found in AI and in dilated EH. The results indicate that nonhypertensive hypertrophy, despite LV mass augmentation, may have normal CR, whereas at a comparable degree of LV hypertrophy, hypertensive hypertrophy has specific reduction in CR. Independent from vascular effects, ventricular dilatation may deteriorate CR because of an abnormal component of coronary vascular resistance.
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PMID:Coronary hemodynamics in hypertensive heart disease: basic concepts and clinical consequences. 240 73

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

This study analyzes and compares systemic and coronary hemodynamics in patients with essential hypertension in relation to hypertrophic heart disease of nonhypertensive origin. Left ventricular function (as assessed from the cardiac index, stroke volume index, ejection fraction, mean velocity of circumferential fiber shortening, mean normalized systolic ejection rate, and isovolumic indexes) may be normal in patients with hypertensive hypertrophy, even with a large increase in muscle mass and in the presence of concomitant coronary artery disease. Left ventricular function is impaired when regional contraction abnormalities or ventricular dilatation, or both, occur and is inversely related to both cardiac size and systolic wall stress. Coronary blood flow (+ 18%), coronary resistance (+ 38%), and myocardial oxygen consumption (MVO2) (+ 21%) are increased in essential hypertension. Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. Coronary reserve may remain normal in both moderate and excessive hypertrophy, provided systolic wall stress and hence the myocardial oxygen consumption are not increased. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption.
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PMID:The coronary circulation in hypertensive heart disease. 624 Apr 56

Cardiovascular function and structure were evaluated by M-mode echocardiography and systemic hemodynamics in paired lean and obese patients, either hypertensive or normotensive. Compared to lean patients, obese patients had greater left atrial (p less than 0.0001), ventricular (p less than 0.001), and aortic root (p less than 0.002) diameters; posterior and septal wall thickness (p less than 0.001); and ventricular mass, cardiac output, stroke volume, and stroke work (all p less than 0.0001). Hypertensive patients had increased posterior wall thickness, end diastolic wall stress, stroke work (p less than 0.01), and a lower radius to posterior wall thickness ratio indicating concentric hypertrophy (p less than 0.001) when compared to normotensive patients. Cardiac adaptation to obesity consists of left ventricular dilatation and hypertrophy (eccentric hypertrophy) irrespective of arterial pressure levels. In contrast, essential hypertension solely produces concentric hypertrophy. Both obesity and hypertension increase left ventricular stroke work by disparate hemodynamic mechanisms; their presence in the same patient will tax the heart and increase the long-term risk of congestive failure.
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PMID:Dimorphic cardiac adaptation to obesity and arterial hypertension. 665 Oct 22

This work examines whether the 24 h blood pressure (BP) pattern per se might affect the left ventricular structure independently of the pressure level. One hundred subjects with abnormally high office BP readings who had never received any antihypertensive treatment were submitted to 24 h ambulatory BP monitoring and left ventricular echocardiographic assessment. They were classified into two groups, as follows: dippers (group 1), consisting of 46 subjects whose mean nighttime systolic BP was reduced by at least 10% in comparison to the corresponding daytime value, and nondippers (group 2), consisting of 54 subjects whose nighttime BP did not drop or was reduced by < 10%. Left ventricular mass and end-diastolic volume values, both normalized for body surface area, were significantly higher in nondippers (r = 3.12, P < .003, and r = 7.46, P < .001, respectively). The two groups did not differ in diastolic thickness of either intraventricular septum or left ventricular posterior wall (both values normalized for body surface area), in mean 24 h systolic or diastolic or average blood pressure, or in age. In conclusion, in untreated essential hypertension diagnosed on the basis of abnormal office BP readings, the higher incidence of left ventricular mass increase in subjects unable to reduce their blood pressure during the night was more due to left ventricular dilatation than to myocardial wall thickening. The effect of the 24 h BP profile on left ventricular volume appears to be independent of both the BP level and age.
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PMID:24 h blood pressure profile affects the left ventricle independently of the pressure level. A study in untreated essential hypertension diagnosed by office blood pressure readings. 903 24

The present study was designed to detect the arrhythmogenic effect of left ventricular hypertrophy, QTc prolongation and the relationship between the QTc duration and ventricular arrhythmias in patients with left ventricular hypertrophy secondary to essential hypertension. Sixty-eight hypertensive patients (51 male and 17 female, mean age 52+/-6 years) and 30 healthy normotensive subjects (22 male and eight female, mean age 49+/-6 years) were enrolled in the study. The frequency of ventricular arrhythmias was investigated with 24-h ambulatory electrocardiographic monitoring and grade 3 and 4 ventricular arrhythmias according to a modified Lown and Wolf classification were accepted as complex arrhythmias. The echocardiographic features of the patients were divided into five groups as follows: (1) normal left ventricular diameter and wall thickness, (2) concentric left ventricular hypertrophy, (3) asymmetric septal hypertrophy, (4) dilated left ventricle, (5) dilated and hypertrophic left ventricle. The frequency of complex ventricular ectopia and the QTc duration were estimated for each group and compared with Student's t-test. Left ventricular hypertrophy was detected in 38 of 68 patients (56%) with essential hypertension. In patients with left ventricular hypertrophy, the incidence of complex ventricular arrhythmias was two- and fivefold higher compared with patients without left ventricular hypertrophy and with controls, respectively. All of the patients with echocardiographic left ventricular dilatation had experienced complex ventricular arrhythmias. QTc duration correlated positively with left ventricular mass index and left ventricular internal diastolic dimension. The highest QTc intervals were detected in patients with left ventricular hypertrophy and complex arrhythmias. In patients with left ventricular hypertrophy, a QTc duration longer than 380 ms had a sensitivity of 74% and a specificity of 89% for detecting complex ventricular arrhythmias. It is concluded that patients with left ventricular hypertrophy have a higher incidence of complex ventricular arrhythmias and QTc prolongation in those patients can be a good marker for the increased risk of arrhythmias.
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PMID:Significance of QTc prolongation on ventricular arrhythmias in patients with left ventricular hypertrophy secondary to essential hypertension. 968 37

Left ventricular hypertrophy (LVH), a risk factor for cardiovascular morbidity and mortality, is commonly caused by essential hypertension. Three geometric patterns of LVH can be induced by hypertension: concentric remodeling, concentric hypertrophy, and eccentric hypertrophy. Clinical studies suggest that different underlying etiologies, genetic modifiers, and risk of mortality are associated with LVH geometric patterns. Since pressure overload-induced LVH can be modeled experimentally using transverse aortic constriction (TAC) and since C57BL/6J (B6) and 129S1/SvImJ (129S1) strains, which have different baseline cardiovascular phenotypes, are commonly used, we conducted serial echocardiographic studies to assess cardiac function up to 8 wk of post-TAC in male B6, 129S1, and B6129F1 (F1) mice. B6 mice had an earlier onset and more pronounced impairment in contractile function, with corresponding left and right ventricular dilatation, fibrosis, change in expression of hypertrophy marker, and increased liver weights at 5 wk of post-TAC. These observations suggest that B6 mice had eccentric hypertrophy with systolic dysfunction and right-sided heart failure. In contrast, we found that 129S1 and F1 mice delayed transition to decompensated heart failure, with 129S1 mice exhibiting preserved systolic function until 8 wk of post-TAC and relatively mild alterations in histology and markers of hypertrophy at 5 wk post-TAC. Consistent with concentric hypertrophy, our results show that these strains manifest different cardiac responses to pressure overload in a time-dependent manner and that genetic susceptibility to initial concentric hypertrophy is dominant to eccentric hypertrophy. These results also imply that genetic background differences can complicate interpretation of TAC studies when using mixed genetic backgrounds.
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PMID:Cardiac response to pressure overload in 129S1/SvImJ and C57BL/6J mice: temporal- and background-dependent development of concentric left ventricular hypertrophy. 1717 76


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