Hemodynamic hypertrophied left ventricular patterns in systemic hypertension

Simone, Giovanni de; Lorenzo, Luigi Di; Moccia, D; Costantino, G; Buonissimo, S; Divitiis, Oreste de

doi:10.1016/0002-9149(87)90614-x

Cited by 38 publications

(20 citation statements)

References 17 publications

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“…4,5 However, most studies have shown that contractile performance was depressed in hypertrophied patients. 3,6 In our study, the two indices of contractile performance relatively independent from ventricular load, ESSVR, and Ees indexed to myocardial mass, were lower in patients with LVH.…”

Section: Left Ventricular Mass and Contractile Performancementioning

confidence: 99%

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function

Nitenberg¹

2001

American Journal of Hypertension

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Left ventricular hypertrophy (LVH) is a physiologic process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular contractile performance, mechanical efficiency and ventriculoarterial coupling are preserved in hypertensive patients with LVH. To assess the differences between patients with and without LVH, left ventricular contractile performance and the ventriculoarterial coupling were compared in two groups of hypertensive patients with similar body surface area and arterial pressures, and normal pump function: 30 patients with LVH (group 1) and 23 without LVH (group 2). Left ventricular angiography coupled with simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and pressure-volume area (PVA). Myocardial contractile performance, assessed by Ees normalized by myocardial mass and by ESSVR, was lower in group 1 than in group 2 (1.23 Ϯ 0.28 v 1.89 Ϯ 0.48 mm Hg/mL/100 g, and 3.85 Ϯ 0.99 v 5.13 Ϯ 0.56 g/cm 2 /mL, respectively, both P Ͻ .001). Ventriculoarterial coupling evaluated through Ea/Ees ratio, and mechanical efficiency evaluated through EW/PVA ratio, were similar in the two groups (0.53 Ϯ 0.08 v 0.51 Ϯ 0.05, and 0.78 Ϯ 0.03 v 0.80 Ϯ 0.02, respectively, NS). In conclusion, this study shows that ventriculoarterial coupling and mechanical efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in hypertensive patients, the matching between left ventricular performance and arterial load and the energy transfer are preserved either through left ventricular hypertrophy with moderate depression of myocardial contractile performance or through enhancement of myocardial contractile performance in patients with normal left ventricular mass.

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Section: Left Ventricular Mass and Contractile Performancementioning

confidence: 99%

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function

Nitenberg¹

2001

American Journal of Hypertension

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“…Preimaging binomial sequences of nonselective radiofrequency pulses separated by magnetic field gradient pulses produced a SPAMM "grid" of black stripes with initial center-to-center separations of 7 mm (Fig 1). Imaging parameters were TE of 30 milliseconds, TR equal to the RR interval, 5-mm-thick slices, 5 . To obtain data for circumferential shortening measurements, multiphase, multislice, short-axis SPAMM images of the left ventricle were then obtained from 13 milliseconds after the R-wave peak, defined as end diastole to end systole, in LVH subjects.…”

Section: Imaging Protocolmentioning

confidence: 99%

Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.

et al. 1994

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BACKGROUND In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo. METHODS AND RESULTS Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04). CONCLUSIONS In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.

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“…7,8 Myocardial structural adaptation of hypertensive cardiovascular disease occurs early in the course of disease, and increased wall thickening can be found even in adolescents whose blood pressure is between the 75th and the 95th percentile for age, which are values considered within the normal range in adults.9,10 Impaired left ventricular filling, because of decreased relaxation in early diastole, is often pre- The sent in hypertensive patients before other arbitrary criteria of LVH are present, such as posterior wall thickness exceeding 1.1 cm, a ventricular mass exceeding an arbitrary value of 134 g/m2, or equally arbitrary voltage and vector criteria on the electrocardiogram. [11][12][13][14][15] In early hypertensive heart disease, impaired filling is predominantly caused by decreased relaxation during early diastole,16-18 whereas in more severe hypertensive heart disease, compliance during late diastole becomes impaired because of an increase in myocardial wall thickness.…”

Section: Point Of Viewmentioning

confidence: 99%

Antihypertensive therapy--going to the heart of the matter.

Messerli

1990

Circulation

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Hemodynamic hypertrophied left ventricular patterns in systemic hypertension

Cited by 38 publications

References 17 publications

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function

Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.

Antihypertensive therapy--going to the heart of the matter.

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