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PubMed1993

Pacing-induced dilated cardiomyopathy increases left-to-right ventricular systolic interaction.

BACKGROUND: The right ventricle (RV) receives part of its systolic pumping force from the left ventricle through systolic ventricular interaction. The purpose of this study was to determine the effects of dilated cardiomyopathy on left ventricular to right ventricular (LV-to-RV) systolic interaction. METHODS AND RESULTS: Studies were performed in six normal pigs and in six pigs in which dilated cardiomyopathy resulting in congestive heart failure (CHF) was produced with rapid ventricular pacing at 230 beats per minute for 1 week. In all pigs, we rapidly withdrew blood from the LV apex into a prosthetic ventricle in a single beat, which reduced LV systolic pressure without changing RV or LV end-diastolic pressure, and the resultant instantaneous changes in RV systolic pressure and pulmonary artery flow were determined. The LV-to-RV mean systolic interaction gain was calculated as the change from a normal beat to the instantaneous unloaded beat in mean RV systolic pressure divided by the change in mean LV systolic pressure. Mean systolic pressure gain was approximately 2 1/2 times greater (P < .05) in the CHF animals (0.103 +/- 0.018 mm Hg/mm Hg) than in the normal pigs (0.04- +/- 0.011 mm Hg/mm Hg). CONCLUSIONS: These data demonstrate that left-to-right ventricular systolic interaction is significantly greater in dilated cardiomyopathy compared with the normal heart, indicating that the contribution of the left ventricle to RV systolic pressure generation has increased. This is consistent with decreased elastance of the interventricular septum resulting in increased coupling between the ventricles.

Animals↗
PubMed1992

Rigid ring fixation of the mitral annulus does not impair left ventricular systolic function in the normal canine heart.

BACKGROUND: Previous studies suggest that rigid fixation of the mitral annulus with an annuloplasty ring may impair left ventricular (LV) systolic performance. We used load-insensitive indexes of global and regional LV contractile mechanics to test the hypothesis that rigid fixation of the mitral annulus alters LV systolic function. METHODS AND RESULTS: Global and regional LV systolic mechanics were compared in 10 dogs during two mitral annular conditions: rigidly fixed and freely mobile. Carpentier-Edwards annuloplasty rings (20-24 mm) were inserted using a special buttressing suture technique that permitted alternate cinching of the ring down onto the annulus and subsequent removal away from the annulus. Aortic flow was measured with an electromagnetic flow probe, LV pressure by a micromanometer, and LV wall thickness and three near-orthogonal LV endocardial chamber dimensions using piezoelectric crystals during four sequential ring conditions: 1) down, 2) away, 3) down, and 4) away. The following parameters were analyzed during each ring condition to assess global LV systolic function: end-systolic chamber elastance (end-systolic pressure-volume relation), fiber elastance (end-systolic stress-volume relation), preload recruitable stroke work, and myocardial stress-strain relation. Additionally, regional LV systolic performance was assessed using the end-systolic pressure-diameter relation and a regional analog of preload recruitable stroke work. No significant differences in any of these measurements of LV systolic mechanics were observed between the two mitral annular conditions. CONCLUSIONS: Rigid fixation of the mitral annulus alters neither global nor regional LV systolic function in anesthetized, open-chest dogs with normal ventricles.

Animals↗
PubMed1992

Determinants of isolated systolic hypertension in the elderly.

AIM: To study the determinants (or mechanisms) of isolated systolic hypertension in the elderly. METHODS: Pulsatile blood pressure and flow (multisensor catheter) were measured in the ascending aorta and impedance spectra were calculated in 18 subjects undergoing cardiac catheterization. Nine subjects (mean +/- SEM age 58 +/- 1.4 years) had increased aortic systolic (166 +/- 2.3 mmHg, P < 0.001), mean (116 +/- 2.1 mmHg, P < 0.02) and pulse blood pressure (83 +/- 2.1 mmHg, P < 0.001) and normal diastolic blood pressure (84 +/- 2.0 mmHg, NS) and constituted the isolated systolic hypertension group. The other nine age-matched (58 +/- 1.1 years) subjects had normal aortic systolic and diastolic blood pressure and constituted the normotensive control group. RESULTS: Both static (peripheral vascular resistance) and dynamic (characteristic impedance and wave reflection) components of left ventricular external load (aortic input impedance) were elevated in the isolated systolic hypertensives compared to the normotensive subjects; peripheral vascular resistance was 44% higher (P < 0.001), characteristic impedance (index of aortic stiffness) was 107% higher (P < 0.001), the first harmonic of impedance moduli (index of wave reflection) was 57% higher (P < 0.004) and the first impedance moduli minimum was shifted to a higher frequency (from 3.4 +/- 0.2 Hz to 4.2 +/- 0.13 Hz, P < 0.008) in the group with isolated systolic hypertension. CONCLUSIONS: The changes in impedance spectra in the isolated systolic hypertensives indicate that the cross-sectional area of the peripheral vascular bed was reduced and that the aorta and large arteries were stiffer, producing an increased pulse wave velocity and an early return of pulse wave reflection in systole. The marked increase in arterial stiffness in isolated systolic hypertension offset the increase in diastolic blood pressure that would have been expected from an increase in peripheral vascular resistance alone, and early return of the reflected pressure wave augmented aortic pressure throughout systole and accounted for the large increase observed in systolic and pulse pressure in the aorta.

Aged↗
PubMed1998

Influence of changes in arterial blood pressure and peripheral arterial resistance on peak systolic velocity ratio.

BACKGROUND: Peak systolic velocity ratio has been described as a parameter to determine the degree of arterial stenosis. But there is very little information about the influence of changes in arterial blood pressure or peripheral arterial resistance during exercise on the peak systolic velocity ratio. PATIENTS AND METHODS: Peak systolic velocity was calculated before and in arterial stenosis in 35 patients with only single stenosis in the femoral or iliacal arteries under 4 different conditions: a) twice under resting conditions as a control, b) increased blood pressure by arm activation but unchanged peripheral vascular resistance, c) increased blood pressure by leg activation with a reduced peripheral vascular resistance by metabolic vasodilatation, d) decreased blood pressure associated with pharmacologically reduced peripheral resistance (10 mg nifedipine). RESULTS: Peak systolic velocity ratio was: a) 5.8 +/- 3.7 and 5.7 +/- 3.3, b) 5.6 +/- 3.6 (the increase in systolic arterial blood pressure was 20 +/- 3 mmHg), c) 6.3 +/- 4.4 (increase in systolic arterial blood pressure was 21 +/- 3 mmHg), d) 5.6 +/- 3.4 (decrease in systolic arterial blood pressure was 18 +/- 8 mmHg) without being significantly different from each other. The correlation factors of the peak systolic velocity ratios to the angiographic diameter reduction were between 0.737 and 0.847. Although the mean values suggest that there is no influence from the different exercise tests or nifedipine application on the peak systolic velocity ratio single stenosis demonstrated large reproducible differences. CONCLUSION: The influence of changes in arterial blood pressure and peripheral resistance on peak systolic velocity ratio appeared small. But a single stenosis showed large increases or decreases of peak systolic velocity ratio possibly due to vasomotion of the prestenotic or stenotic arterial segment.

Adult↗
PubMed1984

Renin dependency of blood pressure in isolated systolic hypertension.

The role of the renin system in the maintenance of the elevated systolic blood pressure in isolated systolic hypertension was investigated in 31 patients who received long-term treatment with propranolol (120 mg daily) and in another group of 22 patients with isolated systolic hypertension who received a test dose of captopril (25 or 50 mg). The greatest systolic blood pressure decrease (35 +/- 5 mm Hg) by propranolol occurred in the high-renin group (n = 9), and the smallest decrease (3 +/- 2 mm Hg) in the low-renin group (n = 9), whereas in the normal-renin group (n = 13), systolic blood pressure was decreased by propranolol by 22 +/- 5 mm Hg. For all the propranolol-treated patients, the decrement in the systolic blood pressure by propranolol was related to the control plasma renin activity (r = 0.63, p less than 0.01) and to the concurrent change in plasma renin activity (r = 0.70, p less than 0.001). Captopril decreased the systolic blood pressure by 55 +/- 10 mm Hg in the high-renin group (n = 11) and by 17 +/- 5 mm Hg in the normal-renin group (n = 6), whereas the smallest decrease (12 +/- 5 mm Hg) in systolic blood pressure occurred in the low-renin group (n = 5). In all the captopril-tested patients (n = 22), the decrease in systolic blood pressure by captopril was related to the control plasma renin activity (r = 0.75, p less than 0.001). These results indicate that the plasma renin activity value indicates the participation of the renin-angiotensin system in the maintenance of the elevated systolic blood pressure in patients with isolated systolic hypertension.

Adult↗
PubMed2004

Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging.

AIMS: This study was designed to characterise both the systolic and diastolic mechanical properties of regions with different degrees of myocardial ischaemic injury after reperfused acute myocardial infarction (AMI). METHODS AND RESULTS: Fourteen dogs underwent 90-min coronary artery occlusion followed by reperfusion. Image acquisition was performed 24 h after reperfusion using three techniques: tagged, first-pass perfusion and delayed-enhancement magnetic resonance imaging (MRI). Systolic circumferential strain and both systolic and diastolic strain rates were calculated in 30 segments/animal. Transmural AMI segments displayed reduced systolic contractility when compared to subendocardial AMI segments (systolic strain = -2.5 +/- 0.5% versus -6.0 +/- 0.9%, P < 0.01 and systolic strain rate = -0.11 +/- 0.12 versus -0.82 +/- 0.16 s(-1), P < 0.01), and both exhibited significant systolic and diastolic dysfunction compared to remote. Moreover, AMI segments presenting with microvascular obstruction ("no-reflow") displayed further compromise of systolic and diastolic regional function (P < 0.05 for both). Importantly, risk region segments only exhibited diastolic impairment (diastolic strain rate = 1.62 +/- 0.14 versus 2.99 +/- 0.13 s(-1), P < 0.001), but not systolic dysfunction compared to remote 24 h after reperfusion. CONCLUSION: Reversibly injured regions can demonstrate persistent diastolic dysfunction despite complete systolic functional recovery after reperfused AMI. Moreover, the presence of no-reflow entails profound systolic and diastolic dysfunction. Finally, tagged magnetic resonance imaging (MRI) strain rate analysis provides detailed mechanical characterisation of regions with different degrees of myocardial ischaemic injury.

Animals↗
PubMed1999

Assessment of right ventricular function by right ventricular systolic time intervals in acute respiratory failure.

OBJECTIVE: Whether right ventricular systolic time intervals accurately reflect right ventricular function in patients with acute respiratory failure was determined by assessing the correlation between right ventricular systolic time intervals and the right ventricular end-systolic pressure-volume relationship. DESIGN: A prospective study. SETTING: A surgical intensive care unit in a university hospital. PATIENTS: Twenty patients with acute respiratory failure. MEASUREMENTS AND MAIN RESULTS: Right ventricular systolic time intervals were determined by the simultaneous graphic display of the electrocardiogram, the phonocardiogram, and the pulmonary artery pressure curve and were expressed as a ratio of the pre-ejection period/right ventricular ejection time. The total electromechanical systole was measured from the onset of the electrocardiographic wave complex to the pulmonic component of the second heart sound. Right ventricular ejection time was measured from the rapid upstroke of the pulmonary artery pressure curve to the dicrotic notch. Right ventricular ejection fraction, from which right ventricular end-systolic volume was derived, was measured by the thermodilution technique. Pulmonary artery dicrotic notch pressure was used as an estimate of right ventricular end-systolic pressure. Data were collected at the baseline and after one or two alterations in preload, to define the right ventricular end-systolic pressure-volume relationship line. There was an inverse correlation between the pre-ejection period/right ventricular ejection time ratio and the slope of the right ventricular end-systolic pressure-volume relationship line (r2 = .67; p < .0001). When patients were divided into two groups, based on the pre-ejection period/right ventricular ejection time ratio, the slope of the right ventricular end-systolic pressure-volume relationship line was lower in the group with a high pre-ejection period/right ventricular ejection time ratio (p < .0001). No difference in other hemodynamic data, between the two groups, was noted. CONCLUSIONS: These data suggest that right ventricular systolic time intervals reflect right ventricular performance accurately in patients with acute respiratory failure.

Acute Disease↗
PubMed1993

Comparative effects of antihypertensive drugs on systolic blood pressure.

Importance of systolic over diastolic blood pressure measurements: Systolic pressure is known to be a more important independent cardiovascular risk factor than diastolic pressure in subjects over 50 years of age; after that age, a high incidence of two types of systolic hypertension is observed, sustained essential hypertension with a disproportionate increase in systolic pressure and isolated systolic hypertension. Effects of lacidipine on blood pressure in the elderly: The effects of vasodilators on blood pressure have been studied extensively. Recently, lacidipine, nitrendipine and enalapril were compared in a multicenter, randomly allocated, double-blind trial in elderly hypertensive patients with a disproportionate increase in systolic pressure treated for 8 weeks (n = 278). In these patients, supine systolic pressure decreased to a greater extent with lacidipine and enalapril than with nitrendipine, the difference between lacidipine and nitrendipine reaching statistical significance. In another trial, lisinopril produced a greater reduction in systolic pressure than atenolol. Finally, in a study in elderly patients with systolic hypertension, long-acting isosorbide dinitrate induced a selective sustained decrease in systolic pressure. Mechanisms of action of vasodilators: A fall in systolic blood pressure may be produced by vasodilators through a reduction in peripheral resistance with or without an active change in arterial compliance. Dihydralazine-like substances do not increase arterial compliance whereas angiotensin converting enzyme inhibitors, calcium entry blockers and nitrates tend to increase arterial compliance for the same decrease in mean arterial pressure.

Aged↗
PubMed1997

Left Atrial Systolic Performance in the Presence of Elevated Left Ventricular End-Diastolic Pressure: Evaluation by Transesophageal Pulsed Doppler Echocardiography of Left Ventricular Inflow and Pulmonary Venous Flow Velocities.

We recorded left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities by transesophageal pulsed Doppler echocardiography in 25 patients with a ratio of peak atrial systolic to early diastolic LVIF velocity of <1 and a left ventricular end-diastolic pressure (LVEDP) of 15 mmHg or greater, as well as in 30 normal subjects. The group consisted of 14 patients with prior myocardial infarction, 7 with dilated cardiomyopathy, and 4 with cardiac amyloidosis, and were divided into: (1) group A (n = 7): peak atrial systolic LVIF velocity of 40 cm/sec or greater; (2) group B (n = 7): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of 30 cm/sec or greater; and (3) group C (n = 11): peak atrial systolic LVIF velocity of <40 cm/sec and peak atrial systolic PVF velocity of <30 cm/sec. Although LVEDPs in groups B and C were significantly greater than in group A, there was no difference between groups B and C. The mean pulmonary capillary wedge pressure (mPCWP) in group C was significantly greater than in groups A and B, but there was no difference between groups A and B. The difference between LVEDP and mPCWP (LVEDP - mPCWP) in group B was significantly higher than in groups A and C. Dilatation of the left atrium (LA) was seen in all three groups, particularly in groups B and C. There were no differences in peak atrial systolic LVIF velocity and LA volume change during atrial contraction between group A and the control group, and there were no differences in LA volume change and peak second systolic PVF velocity between groups A and B. LA volume change and peak second systolic PVF velocity were significantly less in group C than in groups A and B. Among the four patients whose courses could be observed after medical treatment with diuretic and vasodilator, one changed from group B to A, one from group B to C, one from group C to A, and one remained in group C. Thus, recording of peak atrial systolic LVIF and PVF by transesophageal pulsed Doppler echocardiography permits detailed evaluation of LA systolic performance in the presence of elevated LVEDP. These two variables provide important information for less invasive differentiation of LA afterload mismatch from LA myocardial failure.

Journal Article↗
PubMed1998

Transesophageal Pulsed Doppler Echocardiographic Study of Systolic Flow Velocity Patterns of the Pulmonary Vein in Patients with Atrial Fibrillation.

We recorded pulmonary venous flow velocity in 27 patients with atrial fibrillation using transesophageal pulsed Doppler echocardiography to investigate the cycle length-dependent characteristics and background of early systolic reversal and second systolic forward waves. The study group consisted of 15 patients with mitral stenosis, 5 patients with left atrial myxoma, and 7 patients without underlying organic heart disease; they were compared with 20 normal controls in sinus rhythm. The mean pulmonary capillary wedge pressure was significantly greater in patients with mitral stenosis and left atrial myxoma than in normal controls and in patients with isolated atrial fibrillation. The mean peak velocity of the early systolic reversal wave was also significantly greater in patients with mitral stenosis and left atrial myxoma than in patients with isolated atrial fibrillation. The mean peak velocity of the second systolic forward wave was significantly lower in patients with mitral stenosis and left atrial myxoma than in controls and in patients with isolated atrial fibrillation. The preceding RR interval had significant negative correlations with the peak early systolic reversal velocity, left atrial pressure during closure of the mitral valve, and peak V wave height of the pulmonary capillary wedge pressure in patients with mitral stenosis and left atrial myxoma. In the same patient groups, the preceding RR interval had significant positive correlations with the peak second systolic forward velocity and amplitudes of the mitral annular and interatrial septal motions during ventricular systole. The variations in the peak velocities of the early systolic reversal and second systolic forward waves with the preceding RR interval were smaller in patients with more severe mitral stenosis. In conclusion, early systolic reversal waves of the pulmonary venous flow velocity reflect left atrial pressure, and the second systolic forward waves reflect left atrial filling. Both velocities vary with disease conditions or preceding RR intervals in atrial fibrillation.

Journal Article↗
PubMed1983

Interventricular septal configuration as a predictor of right ventricular systolic hypertension in children: a cross-sectional echocardiographic study.

Abnormal interventricular septal position and motion have been noted in patients with right ventricular pressure overload. The quantitative relationship between this alteration in septal configuration and the severity of right ventricular systolic hypertension has not been previously reported. We used cross-sectional echocardiography to assess the radius of septal curvature at end-diastole, midsystole, and end-systole in 20 normal children and 29 children (ages 2 weeks to 20 years) undergoing cardiac catheterization for a variety of congenital cardiac disorders. The measured septal radius of curvature (r) was normalized by the ideal radius (ri) for the left ventricular cavity area and then expressed as normalized septal curvature [l/(r/ri)]. A slight leftward shift and flattening of the interventricular septum occurred in the course of normal systolic contraction (mean +/- SEM normalized curvature at end-diastole 0.92 +/- 0.03 and at end-systole 0.85 +/- 0.02; p less than .05). Marked exaggeration of this configurational change occurred in patients with right ventricular systolic hypertension (right ventricular systolic pressure greater than 50% systemic pressure), with progressive loss of curvature from end-diastole (0.45 +/- 0.05) to end-systole (0.19 +/- 0.06). Normalized septal curvature correlated well with relative right ventricular systolic pressure at all three sampling periods, with the best correlation at end-systole (r = .86). End-systolic flattening of the interventricular septum thus proved to be a sensitive marker for right ventricular systolic hypertension.

Adolescent↗
PubMed1984

Regional myocardial systolic function. Effects of coronary occlusion and reperfusion.

Intramyocardial pressure and segment length were measured during control conditions, during 30 sec coronary artery occlusion, and during reperfusion in the subendocardial (ENDO) and in the subepicardial (EPI) layers of the left ventricular wall, in 9 open-chest dogs. Under control conditions systolic subendocardial pressure, 179 +/- 11 mmHg, exceeded subepicardial pressure, 97 +/- 9 mmHg (P less than .001); the maximal rate of change of pressure in the subendocardium, 2231 +/- 170 mmHg/sec, was greater than in the subepicardium, 960 +/- 125 mmHg/sec, (P less than .001). Subendocardial systolic shortening, 23 +/- 2% was greater than subepicardial systolic shortening 16 +/- 1% (P less than .001). The maximal rate of systolic shortening in the subendocardium, 32 +/- 5 mm/sec, was also higher than in the subepicardial, 14 +/- 1 mm/sec (P less than .001). When the left anterior descending coronary artery was closed, subendocardial and subepicardial systolic pressures decreased immediately; conversely, appreciable changes in segment length were delayed 10-12 heart beats. After 30 sec of coronary occlusion a 35% reduction was observed in subendocardial and subepicardial systolic pressures, and systolic lengthening occurred. During reperfusion systolic shortening showed a brief overshooting and was back to control after 10 +/- 2 sec in subepicardium and 13 +/- 2 sec in subendocardium. Systolic intramyocardial pressure recovered in 14 +/- 3 sec in EPI and 18 +/- 2 sec in ENDO and subsequently rose above control level. Peak rebound occurred after 50-75 sec of reperfusion and was 27% higher than control in subendocardium and 20% in subepicardium. In 5 dogs the effects of coronary occlusions lasting 5, 15, 30, 45 and 60 sec were investigated. A progressive increase in ischemic depression and reperfusion rebound in subendocardial and subepicardial pressures was observed. These data show that subendocardial and subepicardial are both functionally depressed by coronary occlusion and that subendocardial and subepicardial both contribute to reperfusion hyperkinesis. Systolic intramyocardial pressures persist when shortening is abolished. Ischemic depression and reperfusion rebound of systolic intramyocardial pressures are affected by duration of coronary occlusion.

Animals↗
PubMed2003

Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic.

CONTEXT: Approximately half of patients with overt congestive heart failure (CHF) have diastolic dysfunction without reduced ejection fraction (EF). Yet, the prevalence of diastolic dysfunction and its relation to systolic dysfunction and CHF in the community remain undefined. OBJECTIVES: To determine the prevalence of CHF and preclinical diastolic dysfunction and systolic dysfunction in the community and determine if diastolic dysfunction is predictive of all-cause mortality. DESIGN, SETTING, PARTICIPANTS: Cross-sectional survey of 2042 randomly selected residents of Olmsted County, Minnesota, aged 45 years or older from June 1997 through September 2000. MAIN OUTCOME MEASURES: Doppler echocardiographic assessment of systolic and diastolic function. Presence of CHF diagnosis by review of medical records with designation as validated CHF if Framingham criteria are satisfied. Subjects without a CHF diagnosis but with diastolic or systolic dysfunction were considered as having either preclinical diastolic or preclinical systolic dysfunction. RESULTS: The prevalence of validated CHF was 2.2% (95% confidence interval [CI], 1.6%-2.8%) with 44% having an EF higher than 50%. Overall, 20.8% (95% CI, 19.0%-22.7%) of the population had mild diastolic dysfunction, 6.6% (95% CI, 5.5%-7.8%) had moderate diastolic dysfunction, and 0.7% (95% CI, 0.3%-1.1%) had severe diastolic dysfunction with 5.6% (95% CI, 4.5%-6.7%) of the population having moderate or severe diastolic dysfunction with normal EF. The prevalence of any systolic dysfunction (EF < or =50%) was 6.0% (95% CI, 5.0%-7.1%) with moderate or severe systolic dysfunction (EF < or =40%) being present in 2.0% (95% CI, 1.4%-2.5%). CHF was much more common among those with systolic or diastolic dysfunction than in those with normal ventricular function. However, even among those with moderate or severe diastolic or systolic dysfunction, less than half had recognized CHF. In multivariate analysis, controlling for age, sex, and EF, mild diastolic dysfunction (hazard ratio, 8.31 [95% CI, 3.00-23.1], P<.001) and moderate or severe diastolic dysfunction (hazard ratio, 10.17 [95% CI, 3.28-31.0], P<.001) were predictive of all-cause mortality. CONCLUSIONS: In the community, systolic dysfunction is frequently present in individuals without recognized CHF. Furthermore, diastolic dysfunction as rigorously defined by comprehensive Doppler techniques is common, often not accompanied by recognized CHF, and associated with marked increases in all-cause mortality.

Aged↗
PubMed1996

Clinical significance of the apical late systolic ejection murmur: a new phonocardiographic sign indicating dynamic mid-left ventricular obstruction.

Systolic ejection murmurs of the left heart usually have their peak during early to mid-systole. Few reports have addressed ejection murmurs with their peak at late systole. We evaluated the clinical significance of an apical systolic ejection murmur with a peak intensity during late systole using Doppler and two-dimensional (2-D) echocardiography and phonocardiography. The apical late systolic ejection murmur was observed in 9 of 13 consecutive patients with mid-left ventricular obstruction. We investigated the ejection flow velocity and the timing of maximum velocity at the three different sites of the left ventricle, the left ventricular cavity shape, and the timing of the peak murmur intensity in these nine patients (late-murmur group). The same parameters were also examined in 8 consecutive patients with mid-systolic ejection murmurs (mid-murmur group), 10 with early systolic ejection murmurs (early-murmur group), and 7 controls without murmurs. Patients with aortic stenosis were excluded. The mid-ventricular ejection flow velocity was significantly higher in the late-murmur group than in the other three groups; that of the outflow tract was markedly higher in the mid-murmur group. The ejection flow velocity at the aortic orifice of patients in the early-murmur group was significantly high compared with that of the controls. The timing of the peak murmur intensity in each group correlated with that of the peak flow signal at the corresponding site with maximum velocity. In all patients in the late-murmur group, 2-D echocardiography revealed a systolic narrowing of the cavity at the mid-ventricle. Amyl nitrite inhalation induced a marked increase in the intensity of the murmur without evidence of appearing or increasing mitral regurgitation. It was concluded that the apical ejection murmur with a late systolic peak intensity is a new phonocardiographic sign indicative of dynamic, mid-left ventricular obstruction. This murmur should be differentiated from the mitral regurgitant murmur.

Adult↗
PubMed1997

Transesophageal pulsed Doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combined analysis of transmitral and pulmonary venous flow velocities.

BACKGROUND: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis. HYPOTHESIS: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography. METHODS: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle > or = 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s; (2) Group B (n = 13): their ratio < 1, and PVA > or = 25 mm/s; and (3) Group C (n = 26): their ratio > or = 1. The mean age of patients in Group A was lower than that in Groups B and C. RESULTS: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end-diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B. CONCLUSION: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.

Adult↗
PubMed2001

Left ventricular systolic and diastolic function after anthracycline chemotherapy in childhood.

BACKGROUND: In childhood, late cardiotoxicity is characterized by inappropriately thin wall and consequent increased end-systolic wall stress, but the associations of impaired left ventricular geometry and function occurring under these circumstances need further investigation. HYPOTHESIS: The purpose of this study was to assess anthracycline late effects on the relationships occurring between increased end-systolic stress (ESS) and changes in both M-mode systolic measurements (i.e., endocardial and midwall fractional shortening) and Doppler diastolic indices in the pediatric age. METHODS: The population consisted of 101 children treated with anthracyclines for at least 12 months and 91 healthy children. Using M-mode echocardiography, end-systolic wall stress was calculated as index of afterload, and endocardial and midwall fractional shortening as systolic indices. Doppler transmitral measurements were made as diastolic indices. RESULTS: Patients treated with anthracyclines showed significantly lower relative wall thickness and left ventricular mass index, greater end-systolic wall stress, reduced endocardial and midwall fractional shortening and peak E/A ratio, prolonged deceleration, and isovolumic relaxation times. Direct relationships were found between end-systolic wall stress and both endocardial and midwall shortening. The use of midwall shortening in the relation showed a greater, but not significant increase (from 3 to 6%) in the proportion of patients with depressed systolic function than did endocardial shortening. In the anthracycline group, end-systolic wall stress was also inversely related to relative wall thickness and directly to isovolumic relaxation time. CONCLUSIONS: In childhood, reduced myocardial thickness and increased afterload explain much of systolic and diastolic dysfunction of late anthracycline toxicity. Midwall fractional shortening does not seem to add useful information for identifying subsets of children more prone to the development of heart failure.

Adolescent↗
PubMed1994

Systolic and diastolic function in tricuspid valve atresia before the Fontan operation.

Systolic and diastolic function were assessed at preoperative cardiac catheterization in 6 patients with classic tricuspid atresia and were compared with those in control subjects. All patients had systemic-to-pulmonary shunts. Left ventricular end-systolic and end-diastolic volumes and masses were significantly larger in the patient group; stroke volume and the ratio of volume to mass were also higher, but not significantly. Mean end-diastolic, peak systolic and end-systolic pressures were similar. Mean stress at end-systole and peak systole were significantly higher in the patient group. Operant chamber stiffness tended to be lower than normal, but was not statistically significant, and myocardial stiffness was normal for the patient group also. Indexes of systolic function were compared. The rate-corrected mean velocity of fiber shortening in the patient group was lower and its relation with stress at end-systole was variable with 4 abnormal patients. The ratio of stress at end-systole/end-systolic volume was significantly lower in patients. The duration of hospital stay did not correlate with end-diastolic volume or any parameter. Thus, this study found abnormalities of load-dependent and independent indexes of systolic function with normal diastolic function in young preoperative patients with tricuspid atresia.

Cardiac Catheterization↗
PubMed1991

Noninvasive determination of the left ventricular end-systolic pressure.

To find a noninvasive method for estimating left ventricular end-systolic pressure, 40 patients were studied during cardiac catheterization. Arterial pressure was taken directly from the ascending aorta. Carotid pulse tracing and measurement of blood pressure by cuff sphygmomanometry were taken simultaneously. The tracings were calibrated and left ventricular end-systolic pressure was estimated directly and indirectly. Simple linear regression analysis gave the equations: (1) left ventricular end-systolic pressure direct = 0.56 left ventricular end-systolic pressure indirect + 43.8 (r = 0.61, P = 0.00004), and (2) left ventricular end-systolic pressure direct = 0.39 systolic arterial pressure indirect + 48.8 (r = 0.62, P = 0.00002). To test the accuracy of the technique the study was continued in 40 patients. Left ventricular end-systolic pressure was also estimated by the 2 equations. Left ventricular end-systolic pressure direct was correlated with left ventricular end-systolic pressure estimated by the 2 equations and there was no statistical difference. This noninvasive technique is a bedside method for clinical measurement of left ventricular end-systolic pressure.

Aged↗