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PubMed1984

Evaluation of left ventricular contractile performance utilizing end-systolic pressure-volume relationships in conscious dogs.

The relationship between left ventricular end-systolic pressure and volume has been proposed as a model of left ventricular contraction which may be useful for quantifying inotropic state independent of preload and afterload. Although the model has been well-validated in isolated hearts, systematic evaluation in conscious animals with an intact peripheral circulation has been limited. Accordingly, we derived end-systolic pressure-volume relationships in twelve conscious dogs, chronically instrumented to measure left ventricular pressure and dimensions from endocardial ultrasonic crystals in three orthogonal axes. We examined the linearity of the end-systolic pressure-volume relationship, its response to alterations of inotropic state and the peripheral circulation, and the influence of beta-adrenergic reflexes. End-systolic pressure-volume relationships were constructed by linear regression of end-systolic pressure-volume coordinates produced by transient inferior vena caval occlusions during atrial pacing. The relations were highly linear; of 127 inferior vena caval occlusions, the correlation coefficient was 0.96 +/- 0.05 (mean +/- SD). The slope of the end-systolic pressure-volume relationship was not significantly altered either by a moderate resistive afterload induced by angiotensin II infusion, or by a moderate increase in preload produced by dextran, but was increased from 4.7 +/- 2.3 to 6.5 +/- 2.2 mm Hg/ml (P less than 0.05) in response to the positive inotropic stimulus of dobutamine. The volume intercept at zero end-systolic pressure was unaffected by dextran or dobutamine, but was decreased from 12 +/- 8 to 5 +/- 11 ml (P less than 0.01) by angiotensin II infusion, indicating a leftward shift of the end-systolic pressure-volume relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1989

Systolic direct ventricular interaction affects left ventricular contraction and relaxation in the intact dog circulation.

Changes in right ventricular systolic function directly influence left ventricular systolic function. Most of our knowledge of this systolic direct ventricular interaction comes from studies of isolated hearts, which suggest that changes in right ventricular size only affect left ventricular systolic function at low pressures and volumes. However, almost nothing is known about systolic direct ventricular interaction in a heart functioning in situ as a part of the intact circulation. We used sudden constriction of the pulmonary artery to assess the immediate effect of a change in right ventricular pressure and contraction pattern on left ventricular contraction and relaxation on the beat following the pulmonary artery constriction in anesthetized open-chest dogs. By focusing on this first beat, we were able to avoid the confounding effect of series ventricular interaction, which changes left ventricular filling and, thus, indirectly influences left ventricular function. At baseline left ventricular end-diastolic pressure of 9.6 +/- 2.1 mm Hg (mean +/- SD), sudden pulmonary artery constriction increased left ventricular peak systolic pressure by 3 +/- 2 mm Hg (2% change), left ventricular stroke volume by 2 +/- 2 ml (8% change), and monoexponential time constant of left ventricular pressure fall during relaxation by 9 +/- 6 msec (22% change). This increased left ventricular relaxation time constant was associated with altered regional segment length changes in the posterior and anterior left ventricular free walls during relaxation. We conclude that systolic direct ventricular interaction affects left ventricular systolic function and relaxation under normal conditions in the intact circulation.

Animals↗
PubMed1986

Noninvasive estimation of right ventricular systolic pressure in ventricular septal defect by a continuous wave Doppler technique.

Noninvasive determination of right ventricular systolic pressure was attempted in 27 patients with ventricular septal defect based on the peak velocity of left-to-right shunt flow as measured in the right ventricle by a continuous wave Doppler technique. The systolic pressure gradient between the ventricles (delta p: mmHg) was calculated according to the simplified Bernoulli's formula, delta p = 4 V2, where V (m/sec) is the peak velocity of the left-to-right shunt flow. Right ventricular systolic pressure was determined by subtracting delta p from the systolic blood pressure measured in the upper arm, which was regarded as the left ventricular systolic pressure. The peak velocity of left-to-right shunt flow could be measured in all patients except one with muscular ventricular septal defect, and values ranged from 0.6 to 4.8 m/sec. The peak velocity of left-to-right shunt flow decreased inversely with the increase in right ventricular systolic pressure. The values of right ventricular systolic pressure determined by the continuous wave Doppler technique correlated highly (r = 0.820) with those determined by cardiac catheterization. The peak velocity of left-to-right shunt flow also showed high negative correlations with the pulmonary to systemic pressure ratio (r = -0.876) and pulmonary to systemic resistance ratio (r = -0.855). These results indicate that the continuous wave Doppler technique is clinically useful for determination of right ventricular systolic pressure as well as the pulmonary to systemic pressure ratio and pulmonary to systemic resistance ratio.

Cardiac Catheterization↗
PubMed1986

Pulmonary vein blood flow velocity waveform--with special reference to pulmonary "systolic runoff" in patients with atrial septal defect.

In order to evaluate the magnitude of pulmonary "systolic runoff", we studied the pulmonary vein blood flow velocity waveform by positioning a catheter-tip velocity-pressure transducer into the extraparenchymal pulmonary vein just distal to the left atrium. We recorded blood flow velocity and pressure simultaneously, and subsequently identified the zero blood flow velocity with blood flow velocity level of the pulmonary artery in diastole. Patients with atrial septal defect were used as subjects because of the technical ease although the altered hemodynamics were present. Two kinds of flow velocity waveforms were consistently demonstrated. One was a waveform of two peaks with the first peak in late systole and the second peak in early diastole (n = 9). The other was a waveform of one peak with a summit near the end of systole (n = 5). On the assumption that the blood flow velocity waveform obtained with this method is roughly equivalent to the flow volume waveform, we initiated the second study. The area encompassed between the actual flow velocity waveform and the line of zero flow velocity was divided into two compartments, i.e., ventricular systole (S) and diastole (D). The ratios of the area in systole to the sum of the areas in systole and diastole, i.e., (S)/[S) + (D], which are analogous to the pulmonary "systolic runoff", were 0.45 +/- 0.07 (mean +/- SD, n = 13). This suggests that about 40% of the right ventricular stroke volume flows into the pulmonary veins, the left atrium and a portion of the right atrium through the atrial septal defect during ventricular systole.

Adolescent↗
PubMed1993

Effects of flecainide and propafenone on systolic performance in subjects with normal cardiac function.

Flecainide and propafenone are effective in suppressing both ventricular and supraventricular tachyarrhythmias, but their efficacy is often limited by dose-related side effects. This study was performed to evaluate noninvasively the effects of intravenous flecainide and propafenone on left ventricular systolic function indices in a selected population of 40 subjects (28 men and 12 women; mean age, 25 years) with normal cardiac structure and performance. Echocardiographic indexes of global systolic pump function (ejection fraction [EF] and percentage of fractional shortening [percent FS]) as well as monodimensional parameters of the intraventricular septum (IVS) and left ventricular posterior wall (PW) contractility (percent systolic thickening [percent th] and systolic excursion [ex]) were assessed in all subjects at baseline, immediately after, and in the early recovery (15 min) after randomized injection of either flecainide or propafenone. Heart rate and blood pressure did not significantly change after both drugs. A significant increase (p < 0.001) in left ventricular systolic internal diameter was observed after both flecainide and propafenone; simultaneously a significant decrease of percent FS (p < 0.001), EF (p < 0.001), PW percent thickening (th) (p < 0.001), and PWex (p < 0.001 after flecainide and p < 0.01 after propafenone) was recorded. These changes were comparable and promptly reversible. In analyzing individual data, a marked systolic dysfunction was observed in two patients after intravenous flecainide (percent FS from 37 percent to 17 percent and from 42 percent to 13 percent; EF from 55 percent to 40 percent and from 65 percent to 35 percent, respectively) and in one patient after intravenous propafenone (percent FS from 30 percent to 15 percent; EF from 58 percent to 35 percent). We conclude that both intravenous flecainide and propafenone exhibit mild negative inotropic effects leading to a moderate and reversible reduction of left ventricular systolic performance; however, in some cases, a dramatic impairment of systolic pump function may occur, suggesting careful use of both drugs as first-line agents also in normal subjects; finally, the true incidence of this deleterious effect is still unknown.

Adolescent↗
PubMed2006

Right ventricular systolic function is not depressed in morbid obesity.

BACKGROUND: The increased pulmonary blood volume associated with the increased total blood volume in morbidly obese patients increases pulmonary artery pressure and pulmonary vascular resistance, resulting in increased right ventricular (RV) afterload. Thus, the morbidly obese may develop RV dysfunction owing to the increased RV afterload. We examined this possibility by assessing RV contractile function in morbidly obese patients, using RV end-systolic pressure-volume relationship and RV systolic time intervals. METHODS: Included were 25 morbidly obese patients undergoing gastric bypass surgery under general anesthesia. Pulmonary artery pressure and RV end-systolic volume were measured with a thermodilution pulmonary artery catheter. Pulmonary arterial dicrotic notch pressure was used as an estimate of RV end-systolic pressure. Two data points were used to define RV end-systolic pressure-volume relationship. RV systolic time intervals were determined by simultaneous graphic display of the electrocardiograph, phonocardiograph, and pulmonary artery pressure curve, and were expressed as a pre-ejection period/RV ejection time ratio. RESULTS: The mean slope of right ventricular end-systolic pressure-volume relationship line was 0.54 +/- 0.13 and mean pulmonary vascular resistance 274 +/- 80 dyne.sec.cm(-5).m(-2). The mean pre-ejection period/RV ejection time ratio was 0.4 +/- 0.11. There was an inverse correlation between the pre-ejection/RV ejection time ratio and the slope of RV end-systolic pressure-volume relationship line (R(2)=0.658, P<0.0001). CONCLUSION: Our data indicate that RV function is not depressed in morbid obesity despite increased RV afterload.

Adult↗
PubMed2002

Prevalence of systolic hypertension in cats with chronic renal failure at initial evaluation.

OBJECTIVE: To determine prevalence of systolic hypertension and associated risk factors in cats with chronic renal failure evaluated in first-opinion practice. DESIGN: Prospective study. ANIMALS: 103 cats with chronic renal failure. PROCEDURE: Systolic arterial blood pressure (SABP) was measured with a noninvasive Doppler technique, and cats that had SABP > 175 mm Hg on 2 occasions or that had SABP > 175 mm Hg and compatible ocular lesions were classified as hypertensive. Information from the history (previous treatment for hyperthyroidism, age), physical examination (sex, body weight), routine plasma biochemical analyses (creatinine, cholesterol, potassium, sodium, chloride, and calcium concentrations), and thyroid status were evaluated as potential risk factors for systolic hypertension. Variables associated with systolic hypertension were evaluated by use of logistic regression. RESULTS: 20 (19.4%; 95% confidence interval, 13 to 28%) cats had systolic hypertension. Plasma potassium concentration was significantly and inversely associated with systolic hypertension. CONCLUSIONS AND CLINICAL RELEVANCE: Prevalence of systolic hypertension, although clinically important, was lower than that reported previously. The cause of the inverse association between systolic hypertension and plasma potassium concentration is not yet known.

Animals↗
PubMed2003

Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study.

BACKGROUND: Although hypertension is a principal precursor of congestive heart failure (CHF), the separate relations of systolic, diastolic, and pulse pressure with risk for heart failure have not been fully elucidated. OBJECTIVE: To examine the value of blood pressure predictors of heart failure. DESIGN: Community-based inception cohort study. SETTING: Framingham, Massachusetts. PATIENTS: 2040 free-living Framingham Heart Study participants (mean age, 61 years [range, 50 to 79 years]). MEASUREMENTS: The association of baseline systolic, diastolic, and pulse pressure with risk for incident CHF was examined in 894 men and 1146 women. Framingham Heart Study participants free of CHF at the baseline examination (performed from 1968 to 1973) were monitored for up to 24 years (mean, 17.4 years) for new-onset heart failure. Cox proportional hazards models were used to adjust for age, sex, smoking, left ventricular hypertrophy, body mass index, diabetes mellitus, high-density lipoprotein cholesterol level, and heart rate; hazard ratios and 95% CIs for blood pressure variables were estimated. RESULTS: CHF developed in 234 participants (11.8%) during the follow-up period. All three blood pressure components were related to the risk for CHF, but the relation was strongest for systolic and pulse pressure. A 1-SD (20 mm Hg) increment in systolic pressure conferred a 56% increased risk for CHF (hazard ratio, 1.56 [95% CI, 1.37 to 1.77]); similarly, a 1-SD (16 mm Hg) increment in pulse pressure conferred a 55% increased risk for CHF (hazard ratio, 1.55 [CI, 1.37 to 1.75]). These associations were unrelated to age, duration of follow-up, and initiation of treatment for hypertension during follow-up; they were also observed in patients with systolic hypertension (systolic blood pressure > or = 140 mm Hg) at the baseline examination (hazard ratio, 1.41 [CI, 1.18 to 1.69] for pulse pressure and 1.42 [CI, 1.14 to 1.76] for systolic pressure). CONCLUSIONS: Although each component of blood pressure was associated with risk for CHF, pulse and systolic pressure conferred greater risk than diastolic pressure. Increased pulse pressure may help identify hypertensive patients at high risk for overt CHF who are candidates for aggressive blood pressure control.

Aged↗
PubMed2001

Impaired left ventricular systolic function after a half-ironman race.

OBJECTIVE: To assess the effects of prolonged strenuous exercise in the form of a half-ironman (HI) race (2 km swim, 90 km bike ride and a 21 km run) on left ventricular systolic function. METHODS AND RESULTS: The study participants consisted of nine male triathletes (mean age +/- SD 32+/-5 years) who competed in the Great White North HI race. Two-dimensional transthoracic echocardiograms were obtained two to three days before the HI (prerace), immediately after completion of the HI (postrace) and 24 h after cessation of exercise. Compared with before the race, performing an HI was associated with a decline in systolic blood pressure (prerace 127.2+/-15.0 mmHg compared with after the race 116.1+/-10.2 mmHg, P<0.05), the systolic blood pressure to end-systolic cavity area ratio (a surrogate for left ventricular contractility - prerace 14.3+/-3.0 mmHg/cm(2) compared with postrace 11.0+/-2.2 mmHg/cm(2), P<0.05) and the fractional area change (prerace 54.1+/-3.8% compared with postrace 47.4+/-5.5%, P<0.05). There was also a concomitant increase in heart rate (prerace 56.3+/-9.4 beats/min compared with postrace 74.1+/-10.7 beats/min, P<0.05), the end-systolic cavity area (prerace 9.2+/-2.2 cm(2) compared with postrace 10.8+/-1.9 cm(2), P<0.05) and the end-systolic cavity area to end-systolic myocardial area ratio (prerace 0.39+/-0.08 compared with postrace 0.51+/-0.1, P<0.05), which returned toward baseline values 24 h after cessation of the HI. CONCLUSIONS: Performing an HI appears to be associated with a transient impairment in left ventricular contractility and a subsequent decline in left ventricular systolic function that tends to return toward normal values within 24 h after cessation of exercise.

Adult↗
PubMedDate not supplied

Comparison of arterial systolic pressure variation with other clinical parameters to predict the response to fluid challenges during cardiac surgery.

Prophylactic optimization of stroke volume during surgery has been thought by some to reduce complications following surgery. Mechanical ventilation has been shown to induce variations in systolic systemic arterial blood pressure. Measuring such variations in systolic pressure (SPV) might serve as an attractive method for guiding fluid therapy intraoperatively. It is unknown if variations in systolic pressure following the rapid intravenous administration of a specific volume of fluid would lead to changes in pressure measurements obtained from a pulmonary artery with sufficient sensitivity to predict or guide the need for expansion of the intravascular volume to optimize stroke volume as an index of cardiac function. The purpose of this study was to determine if such measurements of changes in systolic pressures would be useful in optimizing stroke volume. Nineteen patients undergoing cardiac surgery were enrolled in a prospective cohort study. Following induction of general anesthesia, one or more 250 mL boluses of 6% hetastarch were administered. Stroke volume was calculated from the cardiac output obtained by thermodilution using a pulmonary artery catheter. If the patient s stroke volume increased by less than 10% as a result of a given fluid challenge, the patient was classified as a non-responder. However, if the stroke volume increased by more than 10%, the patient was classified as a responder. The variations in systolic pressure and echocardiographic indices were simultaneously measured before and after the administration of each 250 mL fluid bolus. Pulmonary artery occlusion pressure (PAOP) values were significantly lower in patients who responded to fluid boluses (p=0.0085) than in those who did not. Similarly SPV and SPVdown values (defined as the decrease in systolic pressure with ventilation) were significantly greater in the responders (p<0.05). No significant intergroup differences were observed in SPVup (increase in systolic pressure with ventilation) or echocardiographic-derived left ventricular end diastolic area. A PAOP value less than 10 mm Hg predicted a response (sensitivity 68%, specificity 79%). Although significant intergroup differences in the extent of systolic pressure variations were observed, no appropriate threshold values could be determined that would accurately predict the response to a fluid bolus. There is a relationship between SPV and SPVdown values and intravascular volume status. SPV and echocardiographic-derived values did not predict the response to a fluid bolus as well as values obtained from the pulmonary artery catheter.

Blood Pressure↗
PubMed1992

Systolic hypertension in the elderly. Pathophysiology and management.

Isolated systolic hypertension occurs with increased prevalence in the elderly population. It is characterized by reduced vascular compliance, often combined with increased peripheral resistance. These changes are not specific to patients with systolic hypertension, occurring, perhaps to a lesser extent, in the normotensive aging population as well. Systolic hypertension is associated with a risk of cardiovascular morbidity and mortality that possibly exceeds that associated with systolic-diastolic hypertension. However, until the recent report of the Systolic Hypertension in the Elderly Program, the benefit of treatment of this population was undocumented. The Systolic Hypertension in the Elderly Program demonstrated that lowering of blood pressure with a diuretic, combined, when necessary, with a beta blocker, reduced the rate of myocardial infarction and stroke. Other agents may also be effective in lowering blood pressure, although their ability to reduce cardiovascular morbidity and mortality in this population remains to be documented. The results suggest that pharmacologic treatment be considered for patients older than 60 years whose systolic blood pressure remains above 160 mm Hg (with a diastolic pressure below 90 mm Hg). Whether treatment should be recommended for all patients with systolic hypertension, or, alternatively, for only those at higher risk for cardiovascular events, remains controversial.

Adrenergic beta-Antagonists↗
PubMed2006

Dynamic morphologic changes in the normal aortic annulus during systole and diastole.

BACKGROUND AND AIM OF THE STUDY: The three-dimensional motion of semilunar attachment of the leaflet 'annulus' remains obscure. It has been suggested that the aortic root is distensible and moves during the cardiac cycle. In the present study, the aortic root was evaluated using two dimensions. The aortic root, notably motion of the aortic annulus, was evaluated using multidetector computed tomography (MDCT), and a three-dimensional reconstruction of the aortic annulus was performed. METHODS: Twenty-five patients (17 males, eight females) underwent MDCT. None of the patients had aortic root disease, aortic valve disease, bicuspid valve, myocardial infarction or atrial fibrillation. The aortic annulus was measured in systole and diastole, and divided into three parts: the right coronary cusp (RCC), left coronary cusp (LCC) and non-coronary cusp (NCC). The lengths of the aortic annulus, sinus of Valsalva and sinotubular junction (STJ) were also measured in systole and diastole on longitudinal views. RESULTS: The lengths of each aortic annulus part in systole and diastole were as follows. In systole: RCC 41.8 +/- 8.1 mm; LCC 39.3 +/- 5.9 mm; NCC 43.7 +/- 7.1 mm. In diastole: RCC 42.4 +/- 7.0 mm; LCC 38.6 +/- 7.8 mm; NCC 41.5 +/- 7.8 mm. No statistically significant differences were observed between lengths in systole and diastole. The longitudinal lengths of aortic annulus, sinus of Valsalva and STJ at each period were as follows. In systole: aortic annulus 22.5 +/- 2.2 mm; sinus of Valsalva 34.9 +/- 4.3 mm; STJ 28.1 +/- 3.2 mm. In diastole: aortic annulus 22.1 +/- 2.2 mm; sinus of Valsalva 34.4 +/- 4.7 mm; STJ 27.2 +/- 3.1 mm. The length of the STJ in systole was significantly greater than that in diastole. CONCLUSION: In the normal aortic root, no part of the aortic annulus changed length during the cardiac cycle. According to changes in aortic root dimensions, the commissures move outwards during the systolic phase.

Adult↗
PubMed1989

Global and regional left ventricular systolic performance in the in situ ejecting canine heart. Importance of the mitral apparatus.

The importance of the intact mitral apparatus in left ventricular (LV) systolic performance has been indirectly suggested by clinical studies of chordal-preserving mitral valve replacement (MVR) or reconstruction. The importance of the intact mitral apparatus has been clearly demonstrated in isovolumic experimental preparations but has not been demonstrated unequivocally in ejecting hearts. Therefore, this question was assessed independently of load in an in situ, open-chest ejecting canine heart preparation (n = 9). Three orthogonal LV dimensions were measured by sonomicrometry. During MVR with complete chordal preservation, snares were placed around the anterior and posterior papillary muscles. After the hearts were weaned from cardiopulmonary bypass, LV function was assessed by caval occlusion to alter LV preload abruptly. The slopes of the end-systolic--pressure-volume (end-systolic elastance, Ees) and stroke-work--end-diastolic volume (preload-recruitable stroke work, PRSW) relations were used to measure global LV systolic function; similarly, the slopes of the end-systolic--pressure-dimension (regional end-systolic elastance, rEes) and stroke-work--end-diastolic dimension changes in regional LV systolic performance. All chordae were then divided by pulling the snares. Immediate reassessment revealed deterioration of global LV function: Ees declined by 72% (14.1 +/- 11.2 mm Hg/ml [mean +/- SD] vs. 3.9 +/- 3.5 mm Hg/ml, p less than 0.001), and PRSW declined by 39% (129 +/- 37 vs. 79 +/- 29 mm Hg, p = 0.0001). Regional LV function was also adversely affected but somewhat selectively: rEes decreased significantly in all three LV dimensions (p less than or equal to 0.03), but rPRSW decreased significantly (-21%) only in the anteroposterior minor LV axis (89 +/- 19 vs. 70 +/- 15 mm Hg, p = 0.005) and in the septal-lateral axis (-19%, p = NS). These data demonstrate the importance of the intact mitral apparatus on LV systolic performance in ejecting hearts, particularly in the LV regions subtended by the papillary muscles.

Animals↗
PubMed1988

[Systolic clicks in mitral valve prolapse: their pathophysiological relationship to the grade and causes of prolapse].

To re-evaluate the clinical significance of non-ejection systolic clicks in mitral valve prolapse (MVP), 154 patients with idiopathic MVP (idiopathic group) and 54 patients with secondary MVP associated with atrial septal defect (secondary group) were studied using phonocardiography and two-dimensional echocardiography. There was no significant difference in the incidence of systolic clicks between the idiopathic (30%) and secondary (24%) groups. The severer the degree of prolapse, the higher the incidence of systolic clicks in both the groups. A systolic click was observed independently of age in the idiopathic group. In the secondary group, however, a systolic click was not observed in patients under 30 years old and increased with advancing age in frequency. The intensity of systolic click tended to increase in proportion to the increase of severity of prolapse in both the groups. These results suggested that systolic clicks may appear irrespective of the causes of prolapse and that the production and the intensity of systolic clicks may be related to the degree of changes in the mitral valve-chordal system and the degree of prolapse.

Adolescent↗
PubMed1985

[Systolic honk in mitral stenosis: a case report].

This case report describes a mitral systolic honk originating from the mitral valve and adjacent structures in a 52 year-old woman with mitral stenosis. The patient was hospitalized because of dyspnea. Auscultation of the heart revealed a grade 3/6 apical early systolic honk accompanied by an increased first heart sound, an opening snap and a diastolic rumble. The phonocardiogram demonstrated an early systolic honk at a frequency of 115 Hz. Intensity of the honk varied on beat to beat basis, increasing in the short preceding R-R interval compared to that in the long one. The M-mode echocardiogram showed early systolic fluttering of the mitral valve and chordae tendineae at the same frequency as the honk. The two-dimensional echocardiogram showed bulging of the anterior mitral leaflet toward the left atrium in early systole. After treatment with digitalis and diuretics, the early systolic honk disappeared in beats with preceding long R-R intervals (greater than 1100 msec). In beats without the honk, systolic fluttering of the mitral valve was not observed. The genesis of the early systolic honk is analogous to that of the honk audible in mitral or tricuspid valve prolapse. The bulging of the anterior mitral leaflet into the left atrium may produce vibrations of the mitral valve leaflets and adjacent structures.

Chordae Tendineae↗
PubMed1996

Diminished contractile reserve in patients with left ventricular hypertrophy and increased end-systolic stress during Dobutamine stress echocardiography.

Left ventricular hypertrophy (LVH) is associated with decreased contractile response to inotropic stimulation in animal models, but this has not been documented in humans. To determine whether LVH is associated with decreased myocardial contractile reserve, we measured left ventricular mass, heart rate-corrected velocity of circumferential fiber shortening (Vcfc), end-systolic stress, and LV ejection fraction (LVEF) in patients with LVH and increased end-systolic stress (n = 6) and in patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalities). The afterload-dependent indexes of left ventricular systolic performance were normal at baseline and showed significant increases at peak dobutamine dose (LVH group: Vcfc 0.91 +/- 0.11 to 1.76 +/- 0.59, p = 0.006; LVEF 49 +/- 5 to 65 +/- 6, p = 0.001; group without LVH: Vcfc 1.16 +/- 0.24 to 1.99 +/- 0.36, p = 0.001; LVEF 61 +/- 6 to 68 +/- 6, p = 0.05). The Vcfc/ end-systolic stress relation, a load-independent index of myocardial contractility, rose in a dose-dependent fashion in both groups, but the increment was significantly less for patients with LVH (p < 0.02), suggesting a blunted myocardial contractile reserve to inotropic stimulation. The change in heart rate-corrected velocity of circumferential fiber shortening per unit of change in end-systolic stress in each patient at each dobutamine dose showed a linear and inverse relationship. The increment in heart rate-corrected velocity of circumferential fiber shortening for a given reduction in end-systolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and increased end-systolic stress, ventricular performance is maintained at the expense of limited myocardial contractile reserve, and that inotropic stimulation unmasks this abnormality, despite a normal response in LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunction and heart failure.

Adult↗
PubMed1997

Most ovine mitral annular three-dimensional size reduction occurs before ventricular systole and is abolished with ventricular pacing.

BACKGROUND: Conventional surgical thinking indicates that mitral annular (MA) size reduction plays a key role in mitral valve closure, and most MA size and shape changes are thought to occur during left ventricular (LV) systole. The influences of left atrial (LA) and LV systole on MA size and shape, however, remain debated. METHODS AND RESULTS: Eight radiopaque markers were placed equidistantly around the MA and imaged using high-speed simultaneous biplane videofluoroscopy in seven closed-chest, sedated sheep before and during asynchronous LV pacing. Marker images were used to compute the three-dimensional coordinates of each marker every 16.7 ms throughout the cardiac cycle, allowing calculation of three-dimensional MA area, septal-lateral (SL) dimension, and commissure-commissure (CC) dimension under control and LV pacing conditions. Maximum MA area occurred in early diastole, and minimum MA area near end-diastole; maximum area reduction was 12+/-1% (P< or =.001). Interestingly, 89+/-3% of area reduction occurred before LV systole. During this "presystolic" period, SL decreased by 8+/-1% and CC by 2+/-1%; the SL/CC ratio fell from 0.73+/-0.02 to 0.69+/-0.01 (P< or =.005), indicating a less circular shape at end-diastole. With LV pacing, total MA area reduction was similar (13+/-2 versus 12+/-1%, P=NS versus control); however, all MA area reduction occurred during LV systole with minimum MA area occurring at end-systole. Presystolic shortening in both SL and CC dimensions was lost, and presystolic ellipticalization disappeared. CONCLUSIONS: Changes in MA size and shape coincident with LA systole included area reduction and shape change prior to the onset of LV contraction. These presystolic changes vanished when LA systole was absent (LV pacing). Thus, LA systole plays a pivotal role in MA size reduction and shape alteration. The unexpected timing of these MA dynamics should be taken into account during mitral valve reparative procedures.

Animals↗
PubMed1998

Felodipine extended release versus conventional diuretic therapy for the treatment of systolic hypertension in elderly patients. The National Trial Group.

OBJECTIVE: To compare 8 weeks of monotherapy using either felodipine extended release (ER) or a conventional diuretic therapy, triamterene/hydrochlorothiazide (HCTZ), in elderly patients with systolic hypertension. DESIGN: Prospective, randomized, single-blind screening, double-blind treatment, parallel group comparison. SETTING: Twenty-nine general and family practice sites across Canada. PARTICIPANTS: Men and post-menopausal women aged 60 to 85 years, with mild to moderate primary systolic hypertension (systolic blood pressure > 160 mm Hg or blood pressure > 140/ > 90 mm Hg). INTERVENTIONS: Daily doses of either felodipine ER (2.5 mg) or triamterene/HCTZ (25/12.5 mg) for 8 weeks. After the first 4 weeks, the patients who responded to the initial dosage (a reduction in systolic blood pressure of at least 15 mm Hg) or whose blood pressure was controlled on the dosage (systolic blood pressure < 140 mm Hg) continued to take the low dose. Among the others, the daily doses were doubled for the final 4 weeks. OUTCOME MEASURES: Systolic blood pressure before beginning treatment and at the end of the study, as well as adverse events and results of heart rate measurement, clinical chemistry tests, electrocardiograms and physical examinations before and after therapy. RESULTS: Sufficient data for analysis were obtained from 216 patients (86 men and 130 women). Mean seated blood pressure was reduced significantly in both the felodipine group (from 168/91 to 151/84 mm Hg) and the diuretic group (from 168/92 to 147/84 mm Hg). The difference in mean reductions in systolic blood pressure between the groups was 2.2 mm Hg (with a 95% confidence interval of-1.7 to 6.0 mm Hg), which was not significant. Clinical chemistry measurements taken before treatment and at the end of the study showed that more patients in the diuretic group developed abnormal values for blood urea nitrogen, uric acid and creatinine. Other changes were unremarkable. The incidence of adverse events was similar in both groups, but more patients in the felodipine group (9) than in the diuretic group (3) discontinued treatment owing to an adverse event. CONCLUSIONS: Felodipine ER (2.5 to 5 mg daily) is as effective in reducing systolic blood pressure as triamterene/HCTZ (25/12.5 mg to 50/25 mg daily). More patients discontinued felodipine treatment than triamterene/HCTZ treatment owing to adverse events. However, patients receiving triamterene/HCTZ tended to have abnormal levels in clinical chemistry tests; these should be monitored.

Aged↗