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PubMed1991

Systolic hypertension in the elderly.

Historically diastolic blood pressure (BP) rather than systolic BP has been regarded clinically as the more important component related to subsequent hypertensive morbidity and mortality, and treatment has thus been directed towards lowering the diastolic BP. Observational studies across many different populations have related cerebrovascular disease and death more to the systolic BP, which appears selectively to increase as the population ages. Isolated systolic hypertension (ISH), therefore, may be more prevalent as westernized societies become older. Those affected with ISH suffer a two- to fivefold increase in rates of stroke and ischemic heart disease compared to normotensives. Currently no clinical trials data exist for ISH showing the efficacy of antihypertensive therapy upon final morbidity and mortality, but a large-scale multicenter clinical trial, the Systolic Hypertension in the Elderly Program (SHEP), is currently underway in the United States. Results are expected in the early 1990s. If the results of this trial confirm the efficacy of treating ISH, the therapeutic challenge of ISH will be to selectively decrease systolic BP without undue side effects.

Age Factors↗
PubMed1993

Factors affecting the propagation of locally activated systolic Ca transients in rat ventricular myocytes.

A method is described to activate the systolic rise of [Ca2+]i in only one region of a single, isolated cell. This is achieved by applying the calcium chelator BAPTA to the rest of the cell from a pipette. Under control conditions electrical stimulation produced a Ca transient which was uniform throughout the cell. If a BAPTA containing solution was applied to one region of the cell for 100-500 ms before stimulation then there was no systolic Ca transient in that region of the cell. In the rest of the cell, however, the Ca transient was identical to that in control conditions. If BAPTA application was discontinued the Ca transient was normal throughout the cell on the next stimulation. In the presence of ouabain the locally activated systolic Ca transient propagated through the cell. Propagation was associated with an increase of systolic but not diastolic [Ca2+]i. These results show that the systolic Ca transient propagates if the cell Ca content is elevated. We suggest that the fact that Ca-overload produces spontaneous Ca release may be due to the fact that it allows spontaneous Ca release (which may always be occurring) to propagate.

Animals↗
PubMed1993

Left ventricular pressure transmission to myocardial lymph vessels is different during systole and diastole.

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pressure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were cannulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip pressure transducer. To obtain the systolic sensitivity, left ventricular pressure was changed by clamping the descending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069 +/- 0.013, n = 213, diastole: 0.76 +/- 0.16, n = 249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. During long diastoles lymph pressure variations are on average 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph vessels within the myocardium is such that volume variations by cardiac contraction are limited.

Animals↗
PubMedDate not supplied

Systolic coronary flow reduction in the canine heart in situ: effects of left ventricular pressure and elastance.

In the externally perfused coronary bed of the isolated heart, LV elastance (Elv) rather than LV pressure (Plv) appears to be the major factor responsible for systolic coronary flow reduction, although effects of both have been demonstrated. However, normal perfusion in the presence of intact autoregulation in the heart in situ may modify these effects. To investigate the systolic coronary flow (Qsyst) responses to changes in end-systolic Elv and in systolic Plv in the intact coronary bed, we studied 7 anesthetized dogs. Dogs were vagotomized, paced and instrumented with Doppler flow probes. Elv, obtained from micromanometer- and conductance-catheters, was changed by dobutamine infusion (10 micrograms/kg/min) and characterized by its slope (Ees) and volume position at 15 kPa (V15). Plv was changed stepwise by volume loading. Correction for metabolism induced changes in Qmean was made. Thus, we found that dobutamine increased Ees by 44% (p < 0.0001), decreased V15 by 43% (p < 0.0001), and reduced corrected Qsyst significantly (p < 0.001) from 22.8 to 13.8 ml/min, while Plv (9.5-19.5 kPa) did not affect corrected Qsyst (p > 0.5). We conclude that systolic coronary flow reduction is related to both elastance parameters, Ees and V15, and not to Plv in the normally perfused canine heart in situ.

Animals↗
PubMed1996

Assessment of systolic and diastolic LV function by MR myocardial tagging.

Heart failure has been divided into several different forms depending on etiology, clinical course and pathophysiology of left ventricular (LV) dysfunction. Systolic and diastolic dysfunction are characterized by a reduced cardiac output with normal (= diastolic dysfunction) or depressed (= systolic dysfunction) LV pump function. New diagnostic techniques such as magnetic resonance imaging (MRI) allow to determine noninvasively LV 3D motion by labelling specific myocardial regions (= myocardial "tagging") with a rectangular or radial grid. From the deformation of this grid rotational and translational motion of the heart can be derived. A "wringing" motion of the left ventricle has been described during systole which includes a clockwise rotation at the base and a counterclockwise rotation at the apex. During diastole, an "untwisting" motion has been demonstrated. In the normal heart, diastolic "untwisting" occurs primarily during isovolumic relaxation, analogous to the systolic "wringing" which takes place mainly during isovolumic contraction. A prolongation of the "untwisting" motion was found in the hypertrophied (aortic stenosis) and hibernating myocardium. Thus, heart failure is associated with profound alterations in the mechanical function of the heart which are manifested by changes in systolic "wringing" and diastolic "untwisting" motion.

Animals↗
PubMedDate not supplied

Systolic stress, coronary hemodynamics and metabolic reserve in experimental and clinical cardiac hypertrophy.

The degree of LV hypertrophy may be determined by the relationships between mass-to-volume ratio and systolic wall stress. Systolic wall stress correlates directly with the MVO2 and inversely with LV function. In chronic hypertrophic heart disease (a) normal stress, (b) low stress and (c) high stress hypertrophy may occur. Low stress hypertrophy has normal LV function and normal or decreased MVO2, whereas high stress hypertrophy mostly has depressed function and an increased MVO2. The MVO2 is directly correlated to LV mass. This relationship is influenced by the variable degree of LV mass, by the mass-to-volume ratio and by inotropic interventions. Systolic stress reserve, the ratio of maximum to instantaneous systolic wall stress, averages 4.5. Similar reserves are present for the coronary (4.9) and for the metabolic reserve (4.6). It is concluded that systolic wall stress represents one of the major determinants of LV performance and of myocardial oxygen consumption.

Animals↗
PubMed1987

Left ventricular end-systolic wall stress to volume relationship before and after surgical closure of ventricular septal defect.

Left ventricular function was examined angiographically in 64 patients with ventricular septal defect and 13 postoperative patients with a preoperatively large shunt (postoperative group). The unoperated 64 patients were divided into three groups; small (left-to-right shunt ratio less than 35%), moderate (35%-50%), and large (greater than 50%). The control group consisted of 27 patients with Kawasaki disease. For assessing left ventricular function, left ventricular shape and the end-systolic wall stress to end-systolic volume index ratio, as well as left ventricular ejection fraction were examined. Left ventricular ejection fraction was higher in the small-shunt group (p less than 0.05) than in the control group, but normal in the other groups. Left ventricular end-diastolic shape was normal only in the small-shunt group and more spherical in the other groups. The large-shunt group alone manifested more spherical left ventricular end-systolic shape and lower end-systolic wall stress to end-systolic volume index (p less than 0.001). These findings suggest that the left ventricular dysfunction is present in patients with a left-to-right shunt larger than 50%, but this change was reversible in patients who underwent early repair of ventricular septal defect.

Cardiac Catheterization↗
PubMed1996

Isoflurane and halothane impair both systolic and diastolic function in the newborn pig.

PURPOSE: Volatile anaesthetics have considerable effects on diastolic relaxation in the adult myocardium. We hypothesized that isoflurane (1) and halothane (H) may have even greater effects on diastolic function in the newborn, as the newborn heart has increased passive stiffness and altered calcium handling relative to the adult. Using a newborn pig model, we compared I and H at three clinically relevant concentrations with respect to both systolic and diastolic function. METHODS: Sixteen newborn pigs were randomized for study at control (background fentanyl 100 micrograms.kg-1.hr-1 and 0.5, 1.0 and 1.5 MAC of I (n = 8) or H (n = 8). Temperature, arterial blood gases, and LVEDP were controlled. Left ventricular pressure (LVP) was monitored continuously and LV anterior-posterior dimension was determined by using sonomicrometry crystals. Systolic function was assessed by peak positive dP/dT (dP/dTmax) and the slope of the end-systolic pressure-dimension (ESP-D) relationship. Diastolic relaxation was given by peak negative dP/dT (-dP/dTmax) and the time constant for ventricular relaxation (tau). Left ventricular stiffness was calculated from the slope of the end-diastolic pressure-dimension (EDP-D) relationship. RESULTS: At equal MAC concentrations, I and H were identical in effect for every variable studied. Systolic function was depressed at all anaesthetic concentrations. Control dP/dTmax (I:1815 +/- 561 (SD) mmHg.sec-1, H:1841 +/- 509) decreased to 832 +/- 341 with 1.5 MAC I and 691 +/- 127 with 1.5 MAC H (P < 0.05 vs control). ESP-D slope decreased from 62 +/- 31 mmHg.mm-1 at control to 15 +/- 11 with 1.5 MAC I and from 79 +/- 16 to 37 +/- 15 with 1.5 MAC H (P < 0.05 vs control). Diastolic function was affected only at higher MAC anaesthesia. Control tau increased from 18.0 +/- 6 msec to 29.1 +/- 7.5 with 1.5 MAC I and from 20.8 +/- 5.9 to 30.0 +/- 11.3 with 1.5 MAC H (P < 0.05). EDP-D slope was increased at both 1 and 1.5 MAC anaesthesia. EDP-D slope increased from 0.16 +/- 0.24 mmHg.mm-1 at control to 0.58 +/- 0.46 with I MAC I and from 0.16 +/- 11 to 0.50 +/- 0.35 with 1 MAC H. The -dP/dTmax decreased at every MAC level of anaesthesia. CONCLUSION: These combined systolic and diastolic effects help to explain the increased sensitivity of the newborn myocardium to volatile anaesthetics.

Anesthetics, Inhalation↗
PubMed2003

Inhibition of left ventricular remodelling preserves chamber systolic function in pressure-overloaded mice.

Controversy exists whether the development of left-ventricular hypertrophy (LVH) is a mechanism able to prevent cardiac dysfunction under conditions of pressure overload. In the present study we re-assessed the long-term effects of attenuating LVH by using L- and D-propranolol, which are equally able to inhibit the development of LVH induced by aortic banding. The aortic arch was banded proximal to the left common carotid artery in 71 CD-1 mice that were then assigned randomly to receive L-propranolol, D-propranolol (both 80 mg/kg per day) or vehicle. Concurrently, sham-operated mice were given L-propranolol, D-propranolol or vehicle. LV dimension and performance were evaluated under isoflurane anaesthesia by cine-magnetic resonance imaging, echocardiography and cardiac catheterization up to 8 weeks after surgery. After 2 weeks of pressure overload, the vehicle-treated banded mice had enhanced LV weight, normal chamber size and increased relative wall thickness (concentric hypertrophy), whereas L-propranolol- or D-propranolol-banded mice showed a markedly blunted hypertrophic response, i.e. normal chamber size and normal relative wall thickness, as well as preserved systolic LV chamber function. After 4 weeks, the vehicle-treated banded mice showed LV enlargement with a reduced relative wall thickness (eccentric remodelling) and a clear-cut deterioration in LV systolic function. In contrast, L-propranolol- or D-propranolol-treated banded mice showed normal chamber size with a normal relative wall thickness and preserved systolic function. A distinct histological feature was that in banded mice, L-or D-propranolol attenuated the development of cardiomyocyte hypertrophy but not the attendant myocardial fibrosis. At the 8-week stage, LV dysfunction was present in propranolol-treated banded mice although it was much less severe than in vehicle-treated banded mice. It is concluded that (i) deterioration of LV systolic performance is delayed if LV hypertrophy is inhibited, (ii) banding-induced deterioration of LV systolic function is associated with LV eccentric remodelling and (iii) the antihypertrophic effect of propranolol is due to a selective action on cardiomyocytes rather than on collagen accumulation

Animals↗
PubMed2003

Trials in isolated systolic hypertension: an update.

Isolated systolic hypertension (ISH) has proved to be a powerful predisposing factor for cardiovascular diseases in the elderly. Recent placebo-controlled interventional trials such as the Systolic Hypertension in the Elderly Program (SHEP), the Systolic Hypertension in Europe (Syst-Eur), and the Systolic Hypertension in China (Syst-China) showed that the lowering of systolic blood pressure using a diuretic- or a calcium antagonist-based treatment is associated with a decrease in cardiovascular events. Antihypertensive therapy was found especially effective in preventing stroke in the elderly with ISH. A slowing in the progression of dementia was observed in patients randomized to a calcium antagonist-based treatment. Patients at high cardiovascular risk such as those with diabetes benefited the most from treatment. In another trial performed in patients with left ventricular hypertrophy (Losartan Intervention For Endpoint Reduction ), a subset of patients had ISH. In those patients, an angiotensin II antagonist-based treatment was superior to a b-blocker-based treatment in preventing cardiovascular complications. The experience accumulated in patients with ISH showed that combination therapy is often required to control blood pressure. Overall, the evidence available today indicates that pharmacologic treatment of ISH markedly improves the outcome of elderly patients.

Aged↗
PubMed1988

Effects of electrophysiologic studies resulting in electrical countershock or burst pacing on left ventricular systolic and diastolic function.

To determine the acute effects of electrophysiologic study on left ventricular systolic and diastolic function in patients requiring termination of induced tachyarrhythmias by either electrical countershock or burst pacing, we examined 16 patients (11 men and five women), aged 43 to 78 years (mean 58 +/- 13), undergoing programmed electrical stimulation. Indices of systolic and diastolic left ventricular function were measured by M-mode echocardiography before and within 1 minute after termination of 22 episodes of induced tachyarrhythmias by defibrillation (n = 16) and burst pacing (n = 6). The left ventricular septal and posterior endocardial surfaces were digitized immediately below the mitral valve leaflets, and indices of systolic and diastolic function were calculated. The results showed a significant impairment in both systolic and diastolic function after termination of tachyarrhythmias by defibrillation, as seen by a decrease in the shortening fraction (23.7 +/- 7.6% to 19.8 +/- 7.8%; p less than 0.005) and a decline in the peak rate of increase in left ventricular diameter during diastole called dD/dtmax (87.4 +/- 36.1 mm/sec to 71.5 +/- 28.9 mm/sec; p less than 0.01), respectively. In addition, indices of systolic and diastolic function measured at baseline were predictive of impairment in diastolic function, as seen by modest but highly significant correlations between the absolute change in dD/dtmax after defibrillation versus the peak velocity of fiber shortening (r = -0.69; p less than 0.005) and dD/dtmax (r = -0.60; p less than 0.02) measured at baseline. Left ventricular function after termination of tachyarrhythmias by burst pacing was not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Doppler echocardiographic assessment of the effect of balloon aortic valvuloplasty on left ventricular systolic function.

In order to evaluate the effects of balloon aortic valvuloplasty on left ventricular systolic function and ejection dynamics, Doppler echocardiographic studies were performed on 29 patients before and following valvuloplasty. Continuous wave aortic velocity signals were digitized and (with catheterization laboratory before and after valvuloplasty valve areas) were used to calculate: stroke volume; ejection time; ejection rate; time to 25%, 50%, and 75% ejection; accelerative (onset systole to peak velocity) ejection volume, time, and rate; and decelerative (peak velocity to end systole) ejection volume, time, and rate. Following valvuloplasty, there were no significant changes in heart rate; time to 25%, 50%, and 75% ejection; accelerative ejection time; and decelerative ejection time. There were significant increases in stroke volume, total ejection rate, accelerative ejection volume, decelerative ejection volume, accelerative ejection rate, and decelerative ejection rate, and a significant decrease in total ejection time. Balloon aortic valvuloplasty has a significant effect on the dynamics of left ventricular ejection. There is an increase in stroke volume and a decrease in ejection time, with relatively little effect on early systole, and a more pronounced effect in late systole. There are significant increases in accelerative and decelerative ejection volumes and rates, and a decrease in the time required for the last 25% of ejection. By improving the mobility of calcified leaflets, balloon aortic valvuloplasty may reduce the forces opposing forward blood movement during the decelerative phase of aortic ejection.

Aged↗
PubMed1991

The relationship between systolic anterior motion of the mitral valve and the left ventricular outflow tract Doppler in hypertrophic cardiomyopathy.

In an attempt to investigate the role of left ventricular blood outflow in the generation of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy, we precisely analyzed the temporal relation of SAM and the left ventricular outflow tract (LVOT) systolic Doppler events obtained at the maximal mitral-septal apposition or equivalent area in eight patients with severe SAM, in five patients with mild/moderate SAM, and in seven patients with no SAM, using M-mode and pulsed Doppler echocardiography; the results were compared with those in 10 normal subjects. In all 13 patients with SAM, the timing of SAM generation corresponded to the LVOT Doppler events either between the onset of SAM and the onset of Doppler (r = 0.834, p less than 0.0001) or between the peak of SAM and the peak of Doppler (r = 0.836, p less than 0.0001). The excursion rate of the development of SAM showed a correlation with the LVOT blood outflow acceleration (r = 0.828, p less than 0.0001). The timing of SAM resolution also correlated with the Doppler events, either between the offset of SAM and the offset of Doppler (r = 0.795, p less than 0.001) or the end of SAM and the end of Doppler (r = 0.859, p less than 0.0001). The LVOT blood outflow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p less than 0.013). The LVOT blood outflow acceleration was significantly higher in patients with severe SAM than in patients with mild/moderate SAM or no SAM. This study suggests that the high LVOT blood outflow acceleration in early systole possibly plays an important part in the generation of the Bernoulli pressure drop and results in anterior motion of the mitral valve. At mid-systole, a drag force and/or suction effect of pressure drop produced by continuous outflow blood may sustain the anterior motion of the mitral valve. At late systole, as the blood flow decelerates, the regression of SAM then occurs.

Cardiomyopathy, Hypertrophic↗
PubMed1987

Effect of oral milrinone on end-systolic relations in patients with severe congestive heart failure.

The new inotropic agent milrinone has both vasodilator and inotropic cardiovascular effects, but the importance of these effects in patients with severe congestive heart failure (CHF) is controversial. The left ventricular (LV) end-systolic pressure-diameter relation was used to determine the independent inotropic effect of milrinone. Seven patients with New York Heart Association class III CHF were invasively monitored with right-sided heart catheters and radial arterial lines. M-mode echocardiography was used to measure LV dimensions. The effect of a 10-mg oral dose of milrinone on hemodynamic, echocardiographic and end-systolic variables was determined. End-systolic pressure was measured at the dicrotic notch of the arterial pressure tracing and end-systolic LV dimensions at the time of aortic valve closure. Methoxamine (n = 6) or nitroprusside (n = 1) was used to alter afterload so that the end-systolic pressure-diameter relation could be determined. Arterial vasodilation from milrinone was evidenced by a decrease in mean arterial blood pressure (88 +/- 5 to 77 +/- 2 mm Hg, p less than 0.025) and an increase in cardiac index (from 2.7 +/- 0.2 to 3.2 +/- 0.2 liters/min/m2, p less than 0.025), with no change in heart rate (80 +/- 5 beats/min). Milrinone decreased preload as assessed by the pulmonary artery wedge pressure (from 17 +/- 2 to 10 +/- 2 mm Hg, p less than 0.01) and end-diastolic LV diameter (from 7.4 +/- 0.4 to 7.0 +/- 0.4 cm, p less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location.

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.

Cardiac Volume↗
PubMed1989

Ability of left ventricular stress-shortening relations, end-systolic stress/volume ratio and indirect indexes to detect severe contractile failure in ischemic or idiopathic dilated cardiomyopathy.

The ability of several proposed indirect and direct indexes of left ventricular LV) systolic performance and contractility to detect clinically important LV dysfunction was evaluated in 42 patients with refractory dilated cardiomyopathy studied with right-sided heart catheterization and M-mode echocardiography. Hemodynamic evaluation demonstrated elevated filling pressure (mean pulmonary artery wedge pressure 24 +/- 6 mm Hg) and depressed function (cardiac index 1.68 +/- 0.43 liters/min/m2). Echocardiographic LV end-diastolic dimension (7.3 +/- 1.0 cm), mass (182 +/- 60 gm/m2) and end-systolic stress (163 +/- 44 x 10(3) dynes/cm2) were increased whereas fractional shortening was depressed in all (mean 12 +/- 4%). During follow-up 88% of patients died at a median interval of 16 months after study. Indirect measurements of LV function (mitral E point-septal separation and the ratio of preejection period to LV ejection time) were abnormal in 100 and 88% of patients, respectively. Contractility was classified as depressed in 36 (86%) patients by the end-systolic stress volume index ratio and in 31 (74%) by the relation between fractional shortening and end-systolic stress. In contrast, the relation between end-systolic stress and velocity of circumferential shortening identified only 7 (17%) patients as having subnormal contractility and classified 9 (21%) as having supernormal contractility. Rate correction of velocity of circumferential shortening only modestly improved the ability of the relation to identify depressed contractility (abnormal in 16 patients or 38 percent).

Aged↗
PubMed1990

Left ventricular systolic response to exercise in patients with systemic hypertension without left ventricular hypertrophy.

Supine exercise radionuclide angiography was performed in 367 men to assess left ventricular (LV) systolic response to exercise; 58 had systemic hypertension without LV hypertrophy on a resting electrocardiogram and 309 were normotensive. All patients met the following criteria defining a low pretest likelihood of coronary artery disease: age less than 50 years; normal electrocardiographic response to exercise; absence of typical or atypical chest pain; and exercise heart rate greater than 120 beats/min. Patients taking beta-receptor blockers were excluded. There were no significant differences between hypertensive and normotensive groups in peak exercise heart rate, workload or exercise duration. However, hypertensive patients had significantly higher peak exercise systolic blood pressures and peak exercise rate-pressure products. There were no differences between patients with and without hypertension in resting ejection fraction, peak exercise ejection fraction (hypertensive patients 0.71 +/- 0.01, normotensive patients 0.70 +/- 0.05) or change in ejection fraction at peak exercise (hypertensive patients 0.07 +/- 0.01, normotensive patients 0.07 +/- 0.04). Diastolic and systolic ventricular volumes tended to be smaller in the hypertensive patients, but the difference was not statistically significant. The change in systolic volume with exercise was similar in the 2 groups (hypertensive -10 +/- 3 ml/m2, normotensive -10 +/- 1 ml/m2). In the absence of electrocardiographic evidence of LV hypertrophy, systemic hypertension does not influence LV systolic response to exercise.

Adolescent↗
PubMed1992

Age-related increase in systolic fraction of pulmonary vein flow velocity-time integral from transesophageal Doppler echocardiography in subjects without cardiac disease.

The pulmonary vein flow velocity-time profile would be equivalent to the pulmonary vein flow volume-time profile, provided that the cross-sectional area of the pulmonary vein remains unchanged during 1 cardiac cycle. The systolic fraction of the pulmonary vein flow velocity-time integral, a ratio of velocity-time integral of the S wave to the sum of velocity-time integrals of the S and D waves, represents the ratio of left atrial storage volume to left ventricular stroke volume. This systolic fraction may help early filling of the left ventricle through an appropriate storage of blood and generation of driving pressure in the left atrium. Because early filling of the left ventricle is progressively impaired with age, it was hypothesized that this systolic fraction is increased with age. Forty-four noncardiac surgical patients (age range 17 to 70 years) who underwent transesophageal Doppler echocardiography under general anesthesia were studied, and left upper pulmonary vein flow and mitral inflow velocities were recorded. The ratio of peak velocity of the E wave to that of the A wave of mitral inflow velocity-time profile (y) decreased with age (y = -0.0245 x age + 2.41; r = -0.672, p < 0.01). Systolic fraction (y) increased with age (y = 0.00373 x age + 0.514; r = 0.656, p < 0.01). The age-related increase in the systolic fraction of pulmonary vein flow velocity-time integral may account for the compensation for impaired early filling of the left ventricle in elderly patients.

Adolescent↗