Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

Karlinger, J S; Williams, David E.; Gorwit, Jeffrey; Crawford, Michael H.; O’Rourke, Robert A.

doi:10.1136/hrt.39.11.1239

Cited by 74 publications

(9 citation statements)

References 36 publications

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“…These data are consistent with the result of a previous study (Karliner et al, 1977) which showed that hypertensive patients who were under antihypertensive therapy demonstrated normal left ventricular function.…”

Section: Discussionsupporting

confidence: 95%

Effect of Therapy on Left Ventricular Function in Hypertension

et al. 1980

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1. Twelve untreated hypertensive patients whose blood pressure was 171.8 +/- 5.5 mmHg systolic and 119.7 +/- 3.4 mmHg diastolic (mean +/- SEM) were treated aggressively with diuretics plus other antihypertensive agents. Echocardiograms were performed before, and 2 weeks, 3 months and 6 months after therapy. Blood pressures were lowered to an average of 142/98 mmHg over the 6 month period. 2. Mean velocity of circumferential fibre shortening rose from 1.1 +/- 0.09 to 1.3 +/- 0.06 diameters/s at 2 weeks and remained elevated at the end of 3 months (1.3 +/- 0.03 diameters/s) (P < 0.025), but returned to the control level in 6 months. Similarly, ejection fraction increased significantly during the same period from a control value of 65.1 +/- 4.4 to 73.4 +/- 1.8% (P < 0.025) and persisted in this range at 3 months. At 6 months the ejection fraction had returned to pretreatment levels. There were significant reductions in left ventricular end-systolic and end-diastolic dimensions. Left ventricular mass index decreased from 182.3 +/- 18.3 to 163.8 +/- 12.4 g/m2 after 6 months of therapy. 3. These results indicate that in the early stages of blood pressure reduction there is a temporary increase in ejection phase indices, probably related to afterload reduction. The reduction in the left ventricular mass index suggests that increased cardiac muscle mass due to elevated blood pressure may be partially reversible after long-term reduction in blood pressure.

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Section: Discussionsupporting

confidence: 95%

Effect of Therapy on Left Ventricular Function in Hypertension

et al. 1980

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“…It appears that the ejection fraction is maintained in the normal range in aortic stenosis for a long time. A similar finding was reported for patients with arterial hypertension (18).…”

Section: Discussionsupporting

confidence: 79%

End-systolic pressure-volume and end-systolic stress-volume relationships in patients with aortic stenosis and with normal valvular function

Mehmel¹,

Schwarz²,

Ruffmann³

et al. 1983

Basic Res Cardiol

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In order to study the effect of left ventricular hypertrophy on the endsystolic pressure-volume relationship, three left ventricular angiograms were performed in ten patients with normal valvular function but with varying left ventricular function (group 1) after 0.15 mg/kg propranolol and 1 mg atropine: at rest, after isosorbide-dinitrate at a decreased afterload and after methoxamine at an enhanced afterload. In eight patients with aortic stenosis (group 2) two left ventricular angiograms were performed: at rest and after isosorbide-dinitrate. Heart rate was kept constant by atrial pacing. Left ventricular mass in group 1 was 89 g/m2 and in group 2 180 g/m2. In group 1 the slope k of the end-systolic pressure-volume relation was related to the ejection fraction (EF) at rest: k = 0.024 . e0.072 EF; r = 0.93. In group 2 this relation was shifted to the left (P less than 0.001): k = 0.135 . e0.057 EF; r = 0.81. The relations, however, between the slope k of the end-systolic stress-volume relation and the ejection fraction were close together in group 1 and in group 2 and crossed at an ejection fraction of 67%. It is concluded: 1. In patients with aortic stenosis the end-systolic pressure-volume relation is steeper than in patients without valvular dysfunction at a given ejection fraction, so the relation between the slope k and the ejection fraction is shifted to the left. 2. The end-systolic stress-volume relationship is not altered in patients with aortic stenosis and seems to be advantageous for the evaluation of left ventricles with substantial hypertrophy due to pressure load.

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“…The methods and recording and analyzing techniques have been described earlier "~1 4 The BP was measured in four different situations:…”

Section: Study Protocolmentioning

confidence: 99%

“…14 The ratio between resting laboratory diastolic BP and isovolumetric contraction time (DBP/ ICT) was calculated as a measure of isovolumetnc pressure nse velocity ' 4 Because LV ejection time is influenced by heart rate, this interval also was expressed as a percentage of the expected value at the observed heart rate with the regression equation: LV ejection time = 390 -1.51 x heart rate, which was previously obtained from a control group of middleaged normotensive men.…”

Section: Imentioning

confidence: 99%

Left ventricular wall stress and systolic function in untreated primary hypertension.

Hartford¹,

Wikstrand²,

Wallentin³

et al. 1985

Hypertension

109

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A noninvasive investigation was undertaken in four blood pressure (BP) groups of untreated 49-year-old men derived by screening a random population sample: normotensive men (n = 20) and subjects with borderline (n = 30), mild (n = 45), or moderate BP elevation (n = 24). We here report the findings regarding left ventricular (LV) wall stress, LV wall thickness, and LV systolic function. Although there was an increase in LV wall thickness with hypertension, the raised BP was not compensated for by a sufficient degree of LV wall thickening to keep wall stress within normal limits in the hypertensive groups. Among a subset of individuals with pronounced increase in wall thickness peak systolic wall stress approached the normal range, but end-systolic wall stress was still high. In spite of high wall stress LV systolic function was normal or supranormal in the hypertensive men. The LV ejection phase indices showed a close inverse correlation with end-systolic wall stress (r = -0.67 to -0.84) in all four BP groups, but no correlation or only a weak correlation with peak systolic wall stress (r = 0.18 to -0.40). As judged from the relationship between end-systolic wall stress and ejection phase indices of LV function in the normotensive controls, all hypertensive groups had higher than expected values for LV ejection phase indices, which indicates an increased myocardial contractility secondary to adrenergic stimulation or to a more efficient contractile machinery in the myocardial cells.

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Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

Cited by 74 publications

References 36 publications

Effect of Therapy on Left Ventricular Function in Hypertension

Effect of Therapy on Left Ventricular Function in Hypertension

End-systolic pressure-volume and end-systolic stress-volume relationships in patients with aortic stenosis and with normal valvular function

Left ventricular wall stress and systolic function in untreated primary hypertension.

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