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Severe aortic valve stenosis with preserved and reduced systolic left ventricular function: diagnostic usefulness of the Tei index.

BACKGROUND: In patients with severe aortic valve stenosis (AS), the onset of heart failure is associated with increased mortality and higher operative risk. Heart failure may result from either systolic, diastolic, or "overall" left ventricular dysfunction. The index "isovolumic contraction time and isovolumic relaxation time divided by ejection time" was shown to be a sensitive indicator of "overall" cardiac dysfunction in patients with dilated cardiomyopathy and cardiac amyloidosis. We sought to define the role of the Tei index in patients with severe AS and to validate this index against conventional measures of systolic and diastolic LV function. PATIENTS AND METHODS: Fifty-three participants underwent left heart catheterization for invasive measurement of LV end-diastolic pressure as a marker of diastolic function: 10 AS patients (valve orifice 0.6 +/- 0.2 qcm) with depressed systolic LV function (defined by LV ejection fraction < or = 45% [mean 32% +/- 8%], 7 male/3 female, 72 +/- 10 years old, DAS group), 22 AS patients (valve orifice 0.7 +/- 0.2 qcm) with preserved systolic LV function (ejection fraction > 45% [mean 55% +/- 6%], 13 male/9 female, 71 +/- 11 years old, PAS group) and 21 asymptomatic control participants (ejection fraction > 45% [mean 62% +/- 8%], 14 male/7 female, 66 +/- 8 years old, CON group). Within 24 hours from catheterization, conventional 2-dimensional and Doppler echocardiographic examination including measurement of the Tei index was performed. RESULTS: LV end-diastolic pressure was elevated in the DAS and in the PAS group in comparison with control participants (32 +/- 6 mm Hg and 22 +/- 7 mm Hg vs 11 +/- 4 mm Hg, respectively, P <.01 for both comparisons). DAS patients were in a higher New York Heart Association functional class than PAS patients (3.2 +/- 0.4 vs 2.2 +/- 0.4, P <.001) The Tei index was easily and reproducibly obtained in all study participants. In the DAS group, isovolumic contraction time was prolonged and ejection time was shortened in comparison with the CON group (102 +/- 20 ms vs 52 +/- 15 ms, P <.01; and 235 +/- 44 ms vs 316 +/- 45 ms, P <.01), resulting in a significantly increased Tei index (0.78 +/- 0.28 vs 0.40 +/- 0.11, P <.01). In the PAS group, isovolumic relaxation time was shortened (62 +/- 18 ms vs 81 +/- 26 ms for the CON group, P <.01) and ejection time was prolonged (335 +/- 34 ms vs 316 +/- 45 ms for the CON group, P <.05), resulting in a decreased Tei index (0.29 +/- 0.12 vs 0.40 +/- 0.11, P <.05). Receiver operating characteristic curve analysis for the Tei index yielded an area under the curve of 0.98 +/- 0.03 for separating DAS and PAS patients. Using a Tei index greater than 0.42 as a cutoff, DAS patients were identified with a sensitivity of 100% and a specificity of 91%. CONCLUSION: The Tei index is significantly increased in patients with severe AS and depressed overall cardiac LV function. In AS patients with predominant diastolic dysfunction, in whom systolic function is preserved, the index is decreased in comparison with control patients. The index differentiates between symptomatic AS patients with depressed and less symptomatic AS patients with preserved systolic LV function, and may thus provide relevant information in the work-up and care of such patients.

Aged↗

Postprandial systolic blood pressure and subsyndromal depression.

Changes in systolic blood pressure following the consumption of a standard meal were measured. We hypothesized that larger postprandial drops in systolic blood pressure would be associated with elevated subsyndromal depressive symptomatology. Following an overnight fast, individuals consumed a liquid meal. Blood pressure and pulse were measured preprandially and during the 90-min postprandial period. Several days later, individuals completed a test for depression. Men and women, patients and caregivers, aged 51 to 82 years, were recruited at an outpatient geriatric day care center. Measurements included systolic and diastolic blood pressures, pulse, and Zung Self-Rating Depression Scale. Results showed that the larger the drop in systolic blood pressure, the higher level of somatic depressive symptomatology. This is the first study to identify depressive symptomatology associated with postprandial systolic blood pressure. These results parallel those reported by Perlmuter and Greenberg (Experimental Aging Research, 22, 325-341, 1996) showing that orthostatic changes in systolic blood pressure were associated with elevated subsyndromal depression.

Aged↗

The second peak of the radial artery pressure wave represents aortic systolic pressure in hypertensive and elderly patients.

BACKGROUND: Simultaneous measurement of ascending aorta and radial artery pressure shows that mean and diastolic pressures (DP) are in close agreement in normotensive adults, while systolic pressures (SP) are not. However, in the aortic pressure wave, a second systolic peak appears with increasing age and increases to represent the SP by age 32 yr, while in the radial artery, a second systolic deflection appears by age 40 yr. We suggest that the second radial systolic wave, sometimes seen during radial arterial pressure monitoring in older hypertensives, represents the aortic SP. We set out to evaluate whether the aortic and radial second systolic peaks agree, and since doubts exist about the agreement between aortic and radial DP in elderly hypertensive patients, we also assessed that relationship. METHODS: We compared simultaneously recorded radial and aortic pressures from 21 anaesthetized adult patients using identical fluid-filled pressure measuring systems. CONCLUSIONS: The second radial pressure peak agreed with that in the aorta within a mean of 0.6 (SD 1.5) mm Hg. The difference between DP in the aorta and radial artery was -1.4 (2) mm Hg. The radial-aortic SP and pulse pressure differences were 5.9 (7.6) and 7.3 (7.6) mm Hg, respectively. These results confirm that when the radial artery pressure wave shows a first and second, or only a second systolic shoulder/peak (on the right side of the pressure wave), the second represents the maximal ascending aortic SP, and that the radial and aortic DP are equivalent, even in older hypertensive patients.

Adult↗

Drug treatment of systolic and of diastolic heart failure in elderly persons.

Underlying causes, risk factors, and precipitating causes of heart failure (HF) should be treated. Patients with HF and an abnormal left ventricular ejection fraction (systolic HF) or normal left ventricular ejection fraction (diastolic HF) should be treated with diuretics if fluid retention is present, with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker if the patient cannot tolerate an ACE inhibitor because of cough, angioneurotic edema, rash, or altered taste sensation, and with a beta blocker unless contraindicated. If severe systolic HF persists, an aldosterone antagonist should be added. If HF persists, isosorbide dinitrate plus hydralazine should be added. Calcium channel blockers should be avoided if systolic HF is present. Digoxin should be avoided in men and women with diastolic HF if sinus rhythm is present and in women with systolic HF. Digoxin should be given to men with systolic HF if symptoms persist, but the serum digoxin level should be maintained between 0.5 and 0.8 ng/ml. Cardiac synchronized pacing should be considered in patients with severe systolic HF despite optimal medical therapy, with sinus rhythm, and with ventricular dyssynchrony.

Aged↗

Effects of low-dose antihypertensive therapy in elderly patients with predominant systolic hypertension.

Patients over 60 years of age (M = 70 years) with the predominant systolic form of essential hypertension (systolic blood pressure greater than 160 mm Hg; diastolic blood pressure less than 100 mm Hg) were treated with a combination of low doses of the diuretic chlorthalidone and the centrally-acting sympatholytic agent clonidine. In this randomized double-blind study, patients received either active treatment (n = 14) or placebo (n = 16). Baseline systolic blood pressure in the treatment group averaged 172 mm Hg and was controlled (fall in systolic blood pressure to less than 140 mm Hg or by at least 10%) in 13 of the 14 patients; in eight patients, control was achieved with a single daily dose (given at night) of the clonidine (.1 mg)-chlorthalidone (15 mg) combination. The active drug was significantly superior to placebo in decreasing systolic blood pressure. Changes measured in the standing position did not differ from those in the supine position. Side effects were mild and transient for both the placebo and the treatment groups. Low-dose combination therapy appears to be a highly effective approach for the management of older patients with predominant systolic hypertension of mild-to-moderate degree.

Aged↗

G-estimation of causal effects: isolated systolic hypertension and cardiovascular death in the Framingham Heart Study.

Time-dependent covariates are often both confounders and intermediate variables. In the presence of such covariates, standard approaches for adjustment for confounding are biased. The method of G-estimation allows for appropriate adjustment. Previous studies applying the G-estimation method have addressed effects on all-cause mortality rather than on specific causes of death. In the present study, a method to adjust for censoring by competing risks is presented. The authors used the approach to estimate the causal effect of isolated systolic hypertension on cardiovascular mortality in the Framingham Heart Study, with a 10-year follow-up using data from 1956 to 1970. Arterial rigidity is a major determinant of isolated systolic hypertension and may be a confounder of the relation between isolated systolic hypertension and cardiovascular death. Conversely, isolated systolic hypertension may by itself contribute to stiffening of the vessel wall, and arterial rigidity may therefore also be an intermediate variable in the causal pathway from isolated systolic hypertension to cardiovascular death. While controlling for arterial rigidity and other baseline and time-dependent covariates, isolated systolic hypertension decreased the time to cardiovascular death by 45% (95% confidence interval 3-69).

Adult↗

Left ventricular end-systolic cavity obliteration as an estimate of intraoperative hypovolemia.

BACKGROUND: Transesophageal echocardiography is increasingly used intraoperatively as a monitor of ventricular function and volume. Although obliteration of the left ventricular (LV) cavity at end-systole is interpreted as indicative of intraoperative hypovolemia, this relation has not been demonstrated directly. METHODS: We continuously monitored the LV short axis by using transesophageal echocardiography and determined the relation between acute changes in LV area and hemodynamic variables in 139 patients undergoing elective coronary artery bypass graft surgery. The end-diastolic areas (EDA) and end-systolic areas were calculated during the control state (after anesthetic induction) and during LV end-systolic cavity obliteration. RESULTS: Thirty-nine of 139 patients had episodes of LV cavity obliteration. Mean LV end-systolic area decreased significantly from the control to obliterated state (7.29 +/- 2.56 to 4.00 +/- 1.46 cm2, P = 0.0001). The corresponding mean LV EDA also significantly decreased from the control to obliterated state (18.18 +/- 4.36 to 12.92 +/- 3.74 cm2, P = 0.0001). Mean ejection fraction area increased from 0.609 +/- 0.095 (control) to 0.692 +/- 0.083 (obliteration) (P < 0.0001). Of these 39 episodes, 31 (80%) were associated with a greater than 10% decrease in EDA relative to the initial value after induction of anesthesia and tracheal intubation; 4 (10%) with increases in ejection fraction area only; and an additional 4 (10%) with no substantial change in either the EDA or ejection fraction area. Overall, LV cavity obliteration was not associated with hemodynamic changes. CONCLUSIONS: Our study demonstrates that LV cavity obliteration is rarely preceded by any acute alteration in hemodynamic parameters. Although end-systolic cavity obliteration detected by intraoperative transesophageal echocardiography is frequently associated with decreases in EDA, not every instance of end-systolic cavity obliteration is indicative of decreased left ventricular filling.

Coronary Artery Bypass↗

Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension.

BACKGROUND: Monitoring left ventricular preload is critical to achieve adequate fluid resuscitation in patients with hypotension and sepsis. This prospective study tested the correlation of the pulmonary artery occlusion pressure, the left ventricular end-diastolic area index measured by transesophageal echocardiography, the arterial systolic pressure variation (the difference between maximal and minimal systolic blood pressure values during one mechanical breath), and its delta down (dDown) component (= apneic - minimum systolic blood pressure) with the response of cardiac output to volume expansion during sepsis. METHODS: Preload parameters were measured at baseline and during graded volume expansion (increments of 500 ml) in 15 patients with sepsis-induced hypotension who required mechanical ventilation. Each volume-loading step (VLS) was classified as a responder (increase in stroke volume index > or = 15%) or a nonresponder. Successive VLSs were performed until a nonresponder VLS was obtained. RESULTS: Thirty-five VLSs (21 responders) were performed. Fluid loading caused an overall significant increase in pulmonary artery occlusion pressure and end-diastolic area index, and a significant decrease in systolic pressure variation and delta down (P < 0.01). There was a significant difference between responder and nonresponder VLSs in end-diastolic area index, systolic pressure variation, and dDown, but not in pulmonary artery occlusion pressure. Receiver-operator curve analysis showed that dDown was a more accurate indicator of the response of stroke volume index to volume loading than end-diastolic area index and pulmonary artery occlusion pressure. A dDown component of more than 5 mmHg indicated that the stroke volume index would increase in response to a subsequent fluid challenge (positive and negative predictive values: 95% and 93%, respectively). CONCLUSION: The dDown component of the systolic pressure variation is a sensitive indicator of the response of cardiac output to volume infusion in patient with sepsis-induced hypotension who require mechanical ventilation.

Aged↗

Comparison of the effects on 24-h ambulatory blood pressure of valsartan and amlodipine, alone or in combination with a low-dose diuretic, in elderly patients with isolated systolic hypertension (Val-syst Study).

OBJECTIVE: The aim of this study was to compare the time-effect profiles of a once-daily administration of valsartan and amlodipine, each given alone or in combination with hydrochlorothiazide, in terms of ambulatory blood pressure (BP) and heart rate in elderly patients with isolated systolic hypertension. METHODS: One hundred and sixty-four elderly outpatients with systolic hypertension received valsartan 80 mg (n=79) or amlodipine 5 mg (n=85) once daily for eight weeks, after which the patients with poorly controlled office BP were up-titrated to valsartan 160 mg or amlodipine 10 mg once daily. If their office systolic BP was still >140 mmHg after eight weeks at these doses, 12.5 mg hydrochlorothiazide was added for a further eight weeks. The hourly BP decreases in all of the patients were calculated on the basis of 24-h ambulatory recordings made after the placebo period and at the end of active treatment. The trough/peak ratio and smoothness index were calculated in the responders. RESULTS: Both the valsartan- and amlodipine-based treatments effectively lowered mean 24-h, daytime and night-time systolic ambulatory BP (all p<0.001) without any significant differences between the two regimens. Ambulatory heart rate decreased in the subjects on valsartan and slightly increased in those on amlodipine (the differences in 24-h and daytime heart rate were significant (p=0.008 and 0.002 respectively). Among the 138 responders, the valsartan-based treatment had a greater anti-hypertensive effect during the daytime hours (p=0.02), a difference that was also significant for average 24-h BP (p=0.02). The mean systolic BP trough/peak ratio was 0.56 in the patients on valsartan, and 0.77 in those on amlodipine (NS). The smoothness index was respectively 1.70 and 1.58 (NS). CONCLUSIONS: The present results show that both the valsartan- and amlodipine-based treatments lead to a similar long-term reduction in 24-h systolic BP. However, in treatment responders, valsartan has a greater anti-hypertensive effect during the daytime.

Aged↗

Modulation of CICR has no maintained effect on systolic Ca2+: simultaneous measurements of sarcoplasmic reticulum and sarcolemmal Ca2+ fluxes in rat ventricular myocytes.

1. The effects of modulating Ca2+-induced Ca2+ release (CICR) in single cardiac myocytes were investigated using low concentrations of caffeine (< 500 microM) in reduced external Ca2+ (0.5 mM). Caffeine produced a transient potentiation of systolic [Ca2+]i (to 800 % of control) which decayed back to control levels. 2. Caffeine decreased the steady-state sarcoplasmic reticulum (SR) Ca2+ content. As the concentration of caffeine was increased, both the potentiation of the systolic Ca2+ transient and the decrease in SR Ca2+ content were increased. At higher concentrations, the potentiating effect decayed more rapidly but the rate of recovery on removal of caffeine was unaffected. 3. A simple model in which caffeine produces a fixed increase in the fraction of SR Ca2+ which is released could account qualitatively but not quantitatively for the above results. 4. The changes in total [Ca2+] during systole were obtained using measurements of the intracellular Ca2+ buffering power. Caffeine initially increased the fractional release of SR Ca2+. This was followed by a decrease to a level greater than that under control conditions. The fraction of systolic Ca2+ which was pumped out of the cell increased abruptly upon caffeine application but then recovered back to control levels. The increase in fractional loss is due to the fact that, as the cytoplasmic buffers become saturated, a given increase in systolic total [Ca2+] produces a larger increase in free [Ca2+] and thence of Ca2+ efflux. 5. These results confirm that modulation of the ryanodine receptor has no maintained effect on systolic Ca2+ and show the interdependence of SR Ca2+ content, cytoplasmic Ca2+ buffering and sarcolemmal Ca2+ fluxes. Such analysis is important for understanding the cellular basis of inotropic interventions in cardiac muscle.

Algorithms↗

Prevention and reversal of isolation-induced systolic arterial hypertension in rats by treatment with beta-adrenoceptor antagonists.

1. Rats were made hypertensive by 5 days of continuous isolation in glass metabolic cages; in the text "hypertensive" means having a systolic blood pressure greater than 145 mmHg. 2. Daily intraperitoneal injections of either propranolol (5 mg/kg) or atenolol (5 mg/kg) reduced systolic blood pressure within 3 days and the systolic blood pressure remained low provided that the treatment was continued. 3. Treatment with metoprolol also lowered the systolic blood pressure of isolated rats but only when a larger dose (10 mg/kg) was given. 4. Systolic blood pressure returned to hypertensive levels following withdrawal of treatment after 15 days of isolation. However, following cessation of treatment after 27 days of isolation, the systolic blood pressure did not rise. 5. Rats given propranolol in the drinking water (intake equivalent to a daily dose of 5 mg/kg) before and during isolation did not develop hypertension. 6. The possibility that suppression of sympathetic function by the beta-adrenoceptor antagonists was responsible for these changes is discussed.

Adrenergic beta-Antagonists↗

Cross sectional study of contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in patients admitted with acute dyspnoea.

OBJECTIVE: To assess the comparative contribution of clinical assessment, electrocardiography, and chest radiography to the diagnosis of left ventricular systolic dysfunction in patients admitted to a general medical ward with acute dyspnoea. DESIGN: Prospective cross sectional study. SETTING: Acute medical admissions ward of a teaching hospital. SUBJECTS: 71 randomly selected patients admitted with acute dyspnoea. MAIN OUTCOME MEASURES: Sensitivity and specificity of each investigation and logistic regression analysis of each variable in identifying left ventricular systolic dysfunction. RESULTS: Clinical assessment in this cohort of patients with severe dyspnoea was generally sensitive (sensitivity 81%). Patients were divided into three groups on the basis of clinical assessment. In the first group (37 patients) the diagnosis of systolic dysfunction was clear, in the second (22) it was in doubt, and in the third (12) it was unlikely. The sensitivity of clinical assessment in identifying left ventricular systolic dysfunction was 81% and the specificity was 47%. The specificity of diagnosis was improved by electrocardiography (69%) and chest radiography (92%). Logistic regression analysis showed that isolated pulmonary crepitations were a comparatively poor predictor of left ventricular systolic dysfunction chi 2 = 10.215, P = 0.0014) but that a full clinical examination had reasonable predictive value (chi 2 = 24.82, P < 0.00001). The combination of clinical assessment and chest radiography improved the accuracy of diagnosis (chi 2 = 28.08, P < 0.00001), as did the combination of clinical assessment and electrocardiography (chi 2 = 32.41, P < 0.00001). CONCLUSION: Clinical assessment in patients admitted with acute dyspnoea is comparatively accurate. Patients with abnormal results on chest radiography, electrocardiography, and clinical examination have a high likelihood of having left ventricular systolic dysfunction. Echocardiography contributes little more to the diagnosis in these patients and may be more efficiently directed towards patients in whom the diagnosis is still in doubt after clinical assessment, chest radiography, and electrocardiography.

Acute Disease↗

Vibration white finger and digital systolic pressure during cooling.

A cold provocation test (measurement of finger systolic pressure during combined body and local finger cooling) was performed on 111 male patients exposed to vibration and with a typical history of cold induced white finger. A new method of calculating the test result is described--namely, digital systolic blood pressure in the cooled test finger as a percentage of the systolic pressure in the arm (DP%). The conventional way of calculating the result, the systolic pressure in the cooled test finger as a percentage of the systolic pressure in the test finger when heated to 30 degrees C, corrected for changes in systemic pressure by the use of a reference finger (FSP%), requires the measurement of the systolic pressure in a reference finger. The two ways of calculating the test results give a similar sensitivity (74% for FSP%, 79% for DP% if all histories are regarded as true) but the new method does not require pressure measurements in a reference finger. This makes the test easier to perform and the result easier to understand.

Blood Pressure↗

Effect of intravenous calcitriol on cardiac systolic and diastolic function in patients on hemodialysis.

The systolic and diastolic function of the heart of hemodialysis (HD) patients and the effect of intravenous vitamin D therapy on cardiac function was studied by Doppler and digitized M-mode echocardiography in 10 HD patients before and after 3-4.5 months of calcitriol therapy. Calcitriol was administered intravenously 1-3 times a week at a dose of 1-2 microg after the dialysis sessions. Ten age- and sex-matched healthy controls were also examined echocardiographically. Before calcitriol therapy cardiac wall thicknesses (interventricular septum, posterior wall) and left ventricle (LV) dimensions (end diastolic, end systolic) were greater, and LV diastolic (peak late diastolic velocity, peak early diastolic velocity/peak late diastolic velocity ratio, isovolumic relaxation time) and systolic (fractional shortening) function was impaired in HD patients as compared to controls. The LV posterior wall thickness was related to plasma parathyroid hormone (PTH; r = 0. 70, p = 0.01) in the patients. Calcitriol therapy raised serum ionized Ca from 1.23+/-0.04 to 1.33 +/- 0.04 mmol/l and reduced PTH from 41.1+/-10.7 to 34.2+/-11.7 pmol/l (29+/-11%). Calcitriol therapy did not cause any significant changes in cardiac function in the whole patient group. However, in a subgroup of 5 patients with severe but controllable hyperparathyroidism (PTH >3 times upper normal margin) the LV dimensions and systolic function improved (LV end systolic dimension from 39.0 +/- 4.0 to 31.3 +/- 2.9 mm, p = 0. 03; LV end diastolic dimension from 57.7 +/- 3.1 to 53.4 +/- 3.0 mm, p = 0.06; fractional shortening from 33 +/- 4 to 42 +/- 3%, p = 0. 03). The diastolic indices improved also, but not significantly. In conclusion, left ventricle hypertrophy and systolic and diastolic dysfunction was observed in HD patients. Intravenous calcitriol therapy improved cardiac function in patients with severe secondary hyperparathyroidism.

Adult↗

Effects of chronic administration of sarpogrelate on systolic blood pressure of spontaneously hypertensive rats: comparison with quinapril.

Effects of long-term sarpogrelate (5-HT(2) antagonist) administration on the systolic blood pressure of Wistar-Kyoto normotensive rats (WKYs) and spontaneously hypertensive rats (SHRs) were studied and compared with those of quinapril (ACE-I). Sarpogrelate and quinapril were administered orally for 12 weeks and body and heart weights, systolic blood pressure and the relationships between heart weight and systolic blood pressure were determined. Although both drug treatments caused decreases in the body weight of WKYs and SHRs, only quinapril induced a decrease in the heart weight of SHRs. In addition, quinapril induced a dose-dependent decrease in systolic blood pressure in WKYs and SHRs while sarpogrelate had no effect on systolic blood pressure. Thus, quinapril showed hemodynamic effects on WKYs and SHRs, but the 5-HT(2) antagonists sarpogrelate did not shown such effects, suggesting that 5-HT(2) receptor antagonists may not be important for controlling systolic blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗

Alterations in left ventricular three-dimensional dynamic geometry and systolic function during acute right ventricular hypertension in the conscious dog.

Fifteen chronically instrumented, conscious dogs were studied to determine whether, in the intact circulation, mechanical interactions dictated by the anatomic contiguity of the two ventricles significantly alter left ventricular (LV) dynamic geometry and systolic function during acute right ventricular (RV) hypertension. The three-dimensional geometry of the left ventricle was monitored with three pairs of ultrasonic dimension transducers; ventricular pressures were measured with micromanometers. Data collected during pulmonary artery constriction (RV pressure 68 +/- 8/7 +/- 4 mm Hg) were compared with control data collected at matched heart rates (RV pressure 32 +/- 8/4 +/- 4 mm Hg). During pulmonary artery constriction, mean calculated LV end-diastolic volumes decreased from 69.2 +/- 20.0 to 56.2 +/- 21.3 cm3 (p less than or equal to 0.05). Mean systolic stroke volume decreased from 20.6 +/- 5.5 to 14.0 +/- 6.3 cm3 (p less than or equal to 0.05). These changes were entirely accounted for by alterations in the behavior of the LV septal-free wall minor axis and rearrangements in LV equatorial geometry. When the pulmonary artery was constricted, elongation of the septal-free wall axis occurred during isovolumic systole and was accompanied by a reciprocal decrease in anterior-posterior dimension. Most of the decrease in septal-free wall dimension occurred during relaxation and early diastole rather than during ejection. Mean septal-free wall end-diastolic dimension decreased from 5.45 +/- 0.69 to 4.90 +/- 0.75 cm (p less than or equal to 0.05). The mean systolic decrease in septal-free wall dimension fell from 0.36 +/- 0.18 to 0.14 +/- 0.22 cm (p less than or equal to 0.05). The end-diastolic dimensions and systolic shortening of the LV anterior-posterior minor axis and base-apex major axis were not significantly altered by pulmonary artery constriction. These findings suggest that during acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.

Animals↗

The effect of pericardium on the end-systolic pressure-segment length relationship in canine left ventricle in acute volume overload.

The effect of the pericardium on the end-systolic pressure-segment length relationship in the left ventricle was examined with an ultrasonic miniature gauge in open-chest dogs. In 12 dogs, blood was infused until left ventricular (LV) end-diastolic pressure reached about 20 mm Hg, and then the pericardium was opened widely. In the other 12 dogs a pericardiectomy was performed without blood infusion. Stroke volume was measured in six dogs in the former group and in seven dogs in the latter group. After blood infusion, LV systolic, end-systolic, and end-diastolic pressures increased from 120 +/- 14 to 162 +/- 16 mm Hg (mean +/- SD), from 106 +/- 13 to 146 +/- 17 mm Hg, and from 8 +/- 2 to 19 +/- 2 mm Hg, respectively (all p less than .01). End-systolic and end-diastolic segment lengths increased from 8.9 +/- 2.1 to 10.6 +/- 2.2 mm and from 11.6 +/- 2.5 to 14.9 +/- 2.7 mm, respectively (both p less than .01). After pericardiectomy, the segments were further lengthened by 8.9 +/- 4.4% and by 10.0 +/- 6.2%, respectively (both p less than .01). Heart rate, LV systolic and end-systolic pressures, and peak positive dp/dt did not change, although end-diastolic pressure fell from 19 +/- 2 to 18 +/- 2 mm Hg (p less than .01). Stroke volume rose from 13.1 +/- 3.7 to 23.9 +/- 5.0 ml due to volume loading and further increased by 26.7 +/- 9.0% after pericardiectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Association between the exercise ejection fraction response and systolic wall stress in patients with chronic aortic insufficiency.

We studied the exercise ejection fraction response in 56 patients with chronic aortic insufficiency. All had left ventricular dilatation but preserved resting ejection fraction and minimal or no symptoms. The exercise ejection fraction increased by 0.05 units or greater in 18 (32%) patients (group I), remained within 0.05 units of the resting value in 18 (32%) patients (group II), and fell by 0.05 units or greater in 20 (36%) patients (group III). There were no significant differences among the groups in left ventricular end-diastolic dimension, end-systolic dimension, or fractional shortening by echocardiography or in resting left ventricular volumes and ejection fraction by radionuclide angiography. Left ventricular end-systolic wall stress was significantly higher in group III than in either group I or group II (89 +/- 20 vs 70 +/- 18 and 69 +/- 17 X 10(3) dyne/cm2; p less than .005). At peak exercise there were no differences among groups in systolic blood pressure. However, end-systolic volume increased from 65 +/- 28 to 77 +/- 36 ml/m2 in group III and fell from 50 +/- 21 to 28 +/- 18 ml/m2 in group I during exercise. Thus, at peak exercise end-systolic volume was nearly three times greater in group III than in group I. Although stress could not be determined directly during exercise, the directional changes in its determinants suggest that it also would have been higher in group III patients. A highly significant inverse correlation was present between the ejection fraction response and the change in end-systolic volume (r = -.87, p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗