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PubMed1989

End-systolic pressure as a balance between opposing effects of ejection.

Ejection has previously been thought to exert only negative effects on end-systolic left ventricular pressure, via mechanisms like shortening deactivation and the force-velocity relation. Whether ejection also exerted a positive influence on pressure generation was tested by comparing two successive beats: 1) the last beat of steady-state ejection versus 2) a totally isovolumic contraction at the end-systolic volume. In 12 isolated, blood-perfused canine hearts loaded with a simulated arterial system, ejecting end-systolic pressure exceeded isovolumic pressure by approximately 10 mm Hg when ejection fraction was 0.3. With both higher and lower ejection fractions, the excess of ejecting end-systolic pressure was smaller; beyond an ejection fraction of roughly 0.5, the trend reversed so that ejecting end-systolic pressure fell below isovolumic pressure. The maximum excess in ejecting end-systolic pressure was quite variable (1-17 mm Hg), but the pattern of its variation with ejection fraction was consistent. A correlate of the positive effect of ejection on ventricular pressure was found in the timing of end systole. For an ejection fraction of 0.4, the systolic duration of ejecting beats was approximately 45% longer than in isovolumic beats (range, 23-67%). Potentially, a positive effect of ejection might be due to a residual influence of the stronger activation of cardiac myofilaments early in ejecting systole during which the sarcomeres were at longer lengths than in the isovolumic beat at end-systolic volume (length-dependent activation). A hypothetical model based on this mechanism reproduced both of the positive effects of ejection that were observed: excess end-systolic pressure and prolonged duration of systole. Thus, the approximate load independence of end-systolic pressure could result from the counter balance between opposing influences of ejection.

Animals↗
PubMed1992

[Doppler and echocardiographic study of normal systolic murmurs].

To elucidate the genesis of normal ejection systolic murmurs, we performed phono and Doppler echocardiography in 42 normal subjects. Individuals with hypertension, ST.T changes on ECG, anemia or other cases with definite cardiovascular findings were excluded from the study. Their ages ranged from 22 to 61 years with an average of 48.1 years. They were classified in 2 groups; 9 with Levine 2/6 systolic murmur and 33 without murmur or with 1/6 murmur. Fifteen patients with pure aortic regurgitation or with aortic prosthesis but without significant stenosis, and 7 patients with pulmonic valvular stenosis were served as control. We correlated the intensity and timing of murmur with maximal flow velocity, acceleration time and other parameters. All systolic murmurs were early systolic. Mid-systolic murmur was not noted. Peak of flow velocity increased at the aortic orifice than at the left ventricular outflow tract or pulmonary orifice. Left-sided peak flow velocity occurred earlier than the right-sided peak flow velocity. Early systolic maximal flow velocity of the aorta significantly increased in 9 subjects with murmur than in the remaining 33 without significant murmur. Ejection fraction, hematocrit and body surface area did not differ between the groups with and without significant murmur. Systolic blood pressure and age, however, were higher in subjects with murmur. In aortic valvular disease, systolic murmurs and peak flow signals were early systolic, but in pulmonary stenosis these were mid-systolic in timing. In conclusion, normal ejection systolic murmurs were early systolic and originated at the aortic orifice. Mid-systolic murmurs were unlikely as left-sided murmur in origin. Flow velocity was the most important determinant of the intensity of ejection murmur.

Adult↗
PubMed1995

Hospitalized congestive heart failure patients with preserved versus abnormal left ventricular systolic function: clinical characteristics and drug therapy.

PURPOSE: To compare clinical characteristics of and pharmacologic therapy for hospitalized patients with congestive heart failure (CHF) and left ventricular systolic dysfunction or normal left ventricular systolic function. PATIENTS AND METHODS: Medical records were reviewed for all patients discharged with a principal diagnosis of CHF from a university hospital and a community hospital between September 1, 1991 and August 31, 1992. Pertinent medical history items and prescribed drug therapies at discharge were recorded for each patient's first calendar year admission. Patients were categorized as having either normal left ventricular systolic function or systolic dysfunction based on the results of echocardiography and radionuclide angiography or contrast ventriculogram. RESULTS: Of 298 patients with CHF, 92 (31%) had normal left ventricular systolic function. Patients with normal systolic function were older, were more often women, were less likely to have a history of coronary artery disease, and were more likely to have a history of hypothyroidism than patients with systolic dysfunction. However, the prevalence of clinical characteristics overlapped considerably between the two groups. Among patients with systolic dysfunction, 79% were discharged on a therapeutic regimen of digoxin, 65% on an angiotensin-converting enzyme inhibitor, and 26% on either a beta-blocker or a calcium channel blocker. Among patients with normal systolic function, 50% were discharged on a regimen of a beta-blocker or a calcium channel blocker and 38% were discharged on digoxin. Twenty-six percent of patients with normal systolic function and without a history of atrial fibrillation were discharged on a digoxin regimen. CONCLUSION: Hospitalized CHF patients with normal left ventricular systolic function and those with diminished left ventricular systolic function share many clinical features. Since recommended drug therapy and prognosis differ, our data underscore the importance of diagnostic testing to assess left ventricular systolic function. Drug therapy for CHF patients provides a major challenge for quality-of-care improvement.

Aged↗
PubMed1985

Comparison of left and right ventricular end-systolic pressure-volume relations in congestive heart failure.

A hemodynamic-radionuclide study was performed to compare the relations between end-systolic pressure and volume in the left and right ventricles in 10 patients with biventricular failure, and to correlate the end-systolic pressure-volume slope with baseline variables of systolic function. During nitroprusside or nitroglycerin infusion, or a combination of both, linear relations were found between end-systolic pressure and volume for both ventricles. In 9 of 10 patients, the end-systolic pressure-volume slope was greater for the left ventricle (mean +/- SD 1.12 +/- 0.36 mm Hg X m2/ml) than for the right ventricle (0.46 +/- 0.27 mm Hg X m2/ml) (p less than 0.001). In all 10 patients, the volume-axis intercept of the pressure-volume relation was greater for the left ventricle (82 +/- 66 ml/m2) than for the right ventricle (2 +/- 30 ml/m2) (p less than 0.005). Right ventricular pressure-volume slope correlated weakly with baseline right ventricular ejection fraction (r = 0.69, p less than 0.05), strongly with the baseline right ventricular end-systolic pressure-volume ratio (r = 0.89) and inversely with baseline right ventricular end-systolic volume (r = -0.86). In conclusion, 1) in patients with severe biventricular failure, changes in systolic pressure influence end-systolic volume more strongly in the right than in the left ventricle. 2) For the right ventricle, the slope of the end-systolic pressure-volume relation is directly related to rest indexes of systolic function. 3) The greater the end-systolic volume at rest, the greater the predicted improvement in right ventricular emptying for any vasodilator-induced reduction in pulmonary artery end-systolic pressure.

Adult↗
PubMed1997

Systolic blood pressure and (cardiac) mortality over 15 years after venous coronary bypass surgery.

OBJECTIVE: The aim of the present study was to determine the influence of pre-operative systolic blood pressure and systolic blood pressure 1 and 5 years after venous coronary bypass surgery on subsequent cardiac and non-cardiac mortality. DESIGN: A prospective 15 years follow-up study. PATIENTS: A series of 446 consecutive coronary bypass surgery patients, operated on between April 1976 and April 1977. According to their systolic blood pressure, patients were divided into five groups. MAIN OUTCOME MEASURES: Systolic blood pressure 5 years after surgery, but not pre-operative systolic blood pressure, was an independent predictor of cardiac mortality. RESULTS: Multivariate Cox proportional hazards analysis revealed that pre-operative systolic blood pressure was not associated with cardiac mortality, while higher systolic blood pressure 1 year after surgery showed a trend towards increased cardiac mortality. Systolic blood pressure 5 years after surgery appeared to be a strong independent predictor of cardiac mortality during the subsequent follow-up period. Patients with a systolic blood pressure of 130-139 mmHg had the lowest risk. Compared to this group, the cardiac mortality risk in patients with a systolic blood pressure 5 years after surgery of 140-149 mmHg, 150-159 mmHg and > or = 160 mmHg, was 2.3 (1.2 to 4.6), 3.4 (1.6 to 7.1) and 3.1 (1.4 to 6.5) times higher. Systolic blood pressure < 130 mmHg 5 years after surgery was also associated with a 2.3 times (1.1 to 4.7) times increased risk for cardiac mortality, compared to patients with a systolic blood pressure of 130-139 mmHg. CONCLUSIONS: These findings underline the importance of systolic blood pressure control in the initial years after coronary bypass surgery.

Adult↗
PubMed1980

Mid-systolic closure of the aortic valve in hypertrophic obstructive cardiomyopathy: a pressure-related phenomenon induced by turbulent blood flow.

The purpose of this study was to determine whether mid-systolic closure and opening of the aortic valve in patients with hypertrophic obstructive cardiomyopathy (HOCM) may reflect dynamic changes of pressure induced by turbulent blood flow in the aorta and left ventricular outflow tract. Five patients with HOCM who had echocardiographic evidence of mid-systolic closure of the aortic valve and two patients with HOCM who did not have transient mid-systolic closure of the aortic valve were studied. In patients in whom mid-systolic closure was present, a transient mid-systolic drop of pressure was present in the left ventricular outflow tract, distal to the dynamic intraventricular obstruction, 17 +/- 3 mm Hg (mean +/- SEM) and in the root of the aorta, 16 +/- 4 mm Hg. In these patients the mid-systolic drop of pressure was consistently associated with a high-intensity intracardiac murmur indicative of turbulence. In the two patients in whom mid-systolic closure of the aortic valve was absent, the transient mid-systolic drop of pressure during systole was minimal (average, 3 mm Hg). The transient mid-systolic drop of pressure distal to the intraventricular obstruction can be explained on the basis of decreased pressure energy of the blood due to turbulence. Since total energy is conserved, increased kinetic energy due to turbulence occurs at the expense of a loss in pressure energy. The transient mid-systolic reduction of pressure in the turbulent zone during systole may cause a pressure differential across the open valvular leaflets resulting in a transient closure of the aortic valve.

Aorta↗
PubMed1993

Factors influencing left ventricular systolic function in nonhypertensive morbidly obese patients, and effect of weight loss induced by gastroplasty.

Heart rate and blood pressure were measured, and echocardiography was performed in 39 patients whose actual body weight was greater than twice their ideal body weight to identify factors influencing left ventricular (LV) systolic function in morbidly obese patients and assess the effect of weight loss on LV systolic function. Patients were studied before and after weight loss induced by gastroplasty. The study cohort was 133 +/- 8% overweight before weight loss and 39 +/- 7% overweight at the nadir of weight loss. Before weight loss, LV fractional shortening varied inversely with LV internal dimension in diastole (an indirect index of preload), LV end-systolic wall stress and systolic blood pressure (indexes of afterload). The weight loss-induced change in LV fractional shortening varied directly with the pre-weight loss LV internal dimension in diastole, LV end-systolic wall stress and systolic blood pressure, and inversely with the pre-weight loss LV fractional shortening. The weight loss-induced change in LV fractional shortening varied inversely with the weight loss-induced changes in LV end-systolic stress and systolic blood pressure. In patients with reduced LV fractional shortening (n = 14), weight loss produced a significant increase in LV fractional shortening that was accompanied by a significant decrease in LV internal dimension in diastole, LV end-systolic stress and systolic blood pressure. The results suggest that LV loading conditions have an important role in determining LV systolic function in morbidly obese patients. Improvement in LV systolic function in these patients is closely related to weight loss-induced alterations in LV loading conditions.

Adult↗
PubMed2005

Quantitative assessment of systolic and diastolic ventricular function with tissue Doppler imaging after Fontan type of operation.

BACKGROUND: There is evidence that "inappropriate hypertrophy" of the single left ventricle, which occurs as a result of acute preload reduction, leads to adverse consequences on ventricular function. However, a systematic study of the capability of tissue Doppler imaging (TDI) to assess systolic and diastolic ventricular functions after the Fontan procedure is still missing. METHODS: Twenty-four postoperative patients aged 12-33 years were prospectively evaluated with two-dimensional echocardiography equipped with TDI capabilities. Nineteen age-matched normal subjects were selected as controls. Good-quality echoes for the measurement of ejection fractions were available in 21 patients. Ten patients (group 1) had systolic dysfunction (ejection fraction < 50%), and 11 patients (group 2) had normal systolic function. Peak systolic and diastolic wall velocities were acquired from the two-chamber view in the myocardia and mitral annulus. RESULTS: Compared with controls, the Fontan patients had a significantly reduced peak systolic velocity at wall and annulus sites. A linear correlation existed between ejection fraction and systolic myocardial velocity from the annular sites. Group 1 patients had lower wall velocities and lower annulus velocities both in systole and diastole. Group 2 patients had preserved systolic velocities but decreased regional and annular early diastolic velocities, suggesting impaired filling. Multiple correlation analysis showed a relation between peak early diastolic mitral velocity and ventricular ejection fraction, mean mitral annular motion at systole, mass/volume ratio, and the number of years post Fontan revision. CONCLUSIONS: Myocardial velocities recorded after the Fontan operation give insight into systolic and diastolic ventricular functions. The peak systolic mitral annular velocity correlated well with the ventricular ejection fraction. The peak early diastolic velocity and the ratio between the early and late diastolic mitral annular velocity are reduced and reflect diastolic dysfunction even in the presence of normal systolic ejection fraction.

Adolescent↗
PubMed1997

Effects of left ventricular systolic function on left ventricular diastolic filling patterns in severe mitral regurgitation.

Significant mitral regurgitation (MR) may alter the normal pattern of Doppler detected left ventricular (LV) filling by causing a prominent early filling (E) wave velocity. The manner and extent to which the typical filling pattern of uncomplicated MR is affected by concomitant impaired LV systolic function has not been characterized. Twenty patients with severe LV systolic dysfunction (2-dimensional echocardiographic estimation of ejection fraction < or = 30%) and 21 age- and sex-matched case controls with normal systolic function (ejection fraction > or = 55%) were selected. In addition, 20 subjects with normal LV systolic function and no MR were analyzed as a reference group. Maximal E-wave velocity was increased and highest among MR patients with preserved LV systolic function (124 +/- 37 cm/s) than among those with LV systolic dysfunction (101 +/- 25 cm/s; p <0.05) and normal controls (74 +/- 18 cm/s; p <0.001). Concurrently, A-wave velocity was lowest in patients with systolic dysfunction and MR (47 +/- 23 cm/s; p <0.001) than in patients with normal systolic function and MR (79 +/- 33 cm/s) and normal controls (74 +/- 20 cm/s). Deceleration time of the E wave was longest among those with normal systolic function and MR (203 +/- 41 ms) than among those with systolic dysfunction and MR (152 +/- 35 ms; p <0.001) and normal controls (167 +/- 53 ms; p <0.05). Thus, systolic LV dysfunction in patients with severe MR, compared to patients with MR and normal LV systolic function, is associated with important changes in diastolic inflow velocities, including reduction of the maximal A-wave velocity to a greater extent than the E wave, resulting in an increased E/A ratio and shortening of deceleration time of the E wave.

Aged↗
PubMed1995

Determinants of systolic pressure variation in patients ventilated after vascular surgery.

OBJECTIVE: To discover the predominant determinant of systolic pressure variation during positive-pressure ventilation in mechanically ventilated patients after a vascular surgical procedure. DESIGN: Case control study. SETTING: Postanesthesia care unit at a university hospital. PARTICIPANTS: Eleven patients who were sedated during mechanical ventilation after abdominal aortic surgery. INTERVENTIONS: Radial arterial pressure and airway pressure were simultaneously recorded. The systolic pressure variation was measured as the mean difference between the maximal and minimal systolic pressure values during five consecutive mechanical breaths. The delta down was measured as the difference between the systolic blood pressure during apnea and the minimal values of the systolic pressure after one mechanical breath. The velocity time integral, which is closely related to stroke volume, was measured throughout the systolic pressure measurements. MEASUREMENTS AND MAIN RESULTS: Positive correlation was found between changes in velocity time integral and the magnitude of both systolic pressure variation (r = 0.73) and delta down (r = 0.80). Volume loading did not significantly modify systolic blood pressure. However, it did not significantly decrease systolic pressure variation and delta down. The corresponding changes in velocity time integral provoked by mechanical ventilation decreased significantly as well. CONCLUSIONS: The decrease in systolic pressure provoked by positive-pressure inspiration reflects simultaneous decreases in stroke volume. This suggests that a decrease in left ventricular filling, associated with positive-pressure inspiration, is responsible for systolic pressure variation. This finding confirms the interest in considering systolic pressure variation to provide reliable information about the responsiveness of the heart to preload variations.

Aged↗
PubMed2006

Systolic blood pressure response to exercise testing is related to the risk of acute myocardial infarction in middle-aged men.

BACKGROUND: We assessed the association of systolic blood pressure response to exercise with the risk of an acute myocardial infarction. DESIGN: We conducted a population-based follow-up study. METHODS: This study was based on 1731 middle-aged men without history of coronary heart disease who underwent a cycle ergometer exercise test. Systolic blood pressure was measured every 2 min during a cycle ergometer exercise test in 1731 men followed for 12.7 years on average. A total of 188 acute myocardial infarctions were observed. RESULTS: The total change in systolic blood pressure, the slope of the rise in systolic blood pressure per minute and maximal systolic blood pressure during exercise in quintiles were related to the risk of acute myocardial infarction. Maximal systolic blood pressure of over 230 mmHg was associated with a 2.47 [95% confidence interval (CI) 1.46-4.18] fold risk of acute myocardial infarction, after adjustment for age, other risk factors including the use of antihypertensive medications and systolic blood pressure at rest. Among men with elevated systolic blood pressure at rest, the relative risk for an acute myocardial infarction was 4.31 (95% CI 2.04-9.07) times higher for those who had a steep slope of systolic blood pressure rise (>9.4 mmHg per min of exercise) as compared with those who had a more gradual rise in systolic blood pressure. CONCLUSIONS: Both rate and levels of rise in systolic blood pressure during a progressive exercise test were risk predictors for acute myocardial infarction. These measurements provide an incremental predictive value for an acute myocardial infarction to elevated resting systolic blood pressure, emphasizing the importance of regular blood pressure measurements during exercise testing.

Antihypertensive Agents↗
PubMed1983

Aging and hypertension: hemodynamic implications of systolic pressure trends.

The progressive rise in systolic pressure throughout life is accepted as a phenomenon of "normative aging," although elevated systolic pressure is established as an independent risk factor for untoward cardiovascular events. An analysis of published data for many thousands of individuals indicates comparable average systolic pressure increments of approximately 20 mm Hg between the ages of 40 and 65 years for both normotensives and hypertensives. In both groups there is a disproportionate rise in systolic pressure, that is, systolic increases more than mean and diastolic pressures. In a young person with a normally elastic arterial system an increase in total peripheral resistance (TPR) produces the same increments in systolic, diastolic, and mean arterial pressures; a decrease in arterial distensibility (AD), on the other hand, increases systolic pressure and decreases diastolic pressure to the same extent, leaving mean pressure unchanged. Thus, the proportion of the systolic pressure rise resulting from increased TPR is equal to the increase in the mean pressure (delta mean); the remainder of the increase (delta systolic minus delta mean) is caused by the only other variable that could account for an additional increase in systolic pressure with advancing age, a decrease in AD. Application of this formulation to published blood pressure data shows that in normotensives the ratio of the contribution toward rising systolic pressure of reduced AD to increased TPR is 1:1 between the ages of 40 and 65 years, whereas in hypertensives it is 2:1. Thus, the natural history of essential hypertension, once established, is one of accelerated arterial stiffening, a mechanism that would contribute importantly to the increasing prevalence of "systolic hypertension" with advancing age.

Adult↗
PubMed1988

Dyspnoea of cardiac origin in 67 year old men: (1). Relation to systolic left ventricular function and wall stress. The study of men born in 1913.

The relation between dyspnoea of presumed cardiac origin and disturbed left ventricular systolic function was studied in a group of 67 year old men from the general population of Gothenburg, Sweden. Forty two men with cardiac dyspnoea were identified and 45 controls were randomly selected from a screened cohort of 644 men. Dyspnoea was graded according to the World Health Organisation standard, and M mode echocardiography, carotid pulse tracing, an apex cardiogram, and phonocardiography were used to evaluate the grade of dyspnoea and its relation to systolic time intervals, left ventricular ejection indices, and wall stress. The dyspnoea grade was significantly related to the left ventricular end systolic dimension, to septal and posterior wall fractional thickening, and to ejection indices such as fractional shortening. The dyspnoea grade was also significantly correlated with the ratio of end systolic wall stress to end systolic volume index. There was a close relation between end systolic wall stress and mean velocity of circumferential fibre shortening adjusted for heart rate. This relation did not clearly show reduced inotropy in the dyspnoeic men. There was no relation between the degree of dyspnoea and the systolic time intervals. Among the systolic variables obtained by echocardiography the only abnormal finding in mild to moderate dyspnoea was an increased end systolic dimension. The grade of cardiac dyspnoea seemed to be related to the degree of systolic left ventricular dysfunction, which was considerably impaired in severe dyspnoea. In population studies left ventricular end systolic dimension and fractional shortening may provide sufficient information on systolic function without the need to assess variables that are independent of load.

Aged↗
PubMed2005

Left ventricular systolic performance, function, and contractility in patients with diastolic heart failure.

BACKGROUND: Patients with diastolic heart failure (DHF) have significant abnormalities in left ventricular (LV) diastolic function, including slow and delayed relaxation and increased chamber stiffness. Whether and to what extent these abnormalities in diastolic function occur in association with abnormalities in LV systolic performance, function, and contractility has not been investigated thoroughly. METHODS AND RESULTS: The systolic properties of the LV were examined in 75 patients with heart failure and a normal ejection fraction (ie, DHF) and 75 normal control subjects with no evidence of cardiovascular disease. LV systolic properties were assessed with echocardiographic and cardiac catheterization data. Stroke work (an index of LV systolic performance), preload recruitable stroke work and ejection fraction (indices of LV systolic function), systolic stress-shortening relationship, end-systolic pressure-volume relationship, and peak (+)dP/dt (indices of LV contractility) were examined. The systolic properties of the LV were normal in patients with DHF. Stroke work was 8.4+/-2.3 in DHF versus 8.8+/-2.5 kg . cm in controls (P=0.26). Preload recruitable stroke work was 99+/-22 in DHF versus 109+/-18 g/cm2 in controls (P=0.13). The relationship between stroke work and end-diastolic volume was similar in DHF and controls. Peak (+) dP/dt was 1596+/-362 in DHF versus 1664+/-305 mm Hg/s in controls (P=0.54). The end-systolic pressure-volume relationship was increased in DHF. The systolic stress versus endocardial fractional shortening relationship was similar in DHF and controls. CONCLUSIONS: Patients with DHF had normal LV systolic performance, function, and contractility. The pathophysiology of DHF does not appear to be related to significant abnormalities in these systolic properties of the LV.

Adult↗
PubMed1989

Long-term versus intrabeat history of ejection as determinants of canine ventricular end-systolic pressure.

We studied the effect of ejection on end-systolic pressure in isolated heart preparations. Ejecting beats were compared with isovolumic beats having the same volume as at end systole. While holding end-systolic volume constant, various stroke volumes, including negative stroke volumes (volume injected during systole), were imposed using a predetermined volume command. After switching contraction mode between ejecting and isovolumic, we measured the immediate and steady changes in end-systolic pressure. In the first isovolumic beat after switching from steady-state ejecting beats, the change in end-systolic pressure was variable, depending on the stroke volume. The end-systolic pressure of the ejecting beat exceeded that of the isovolumic beat on average by up to 18 mm Hg with small stroke volume, but the ejecting end-systolic pressure became lower than isovolumic with either large stroke volume (stroke volume/end-systolic volume less than 0.96) or with negative stroke volume. During the transient phase following a switch from ejecting to isovolumic, the end-systolic pressure gradually decreased to a steady state. Consequently, even in steady state, ejecting end-systolic pressure exceeded isovolumic pressure over a significant range of stroke volume (stroke volume/end-systolic volume less than 1.18). After returning contraction mode from isovolumic back to ejecting, we observed responses that were a mirror image. These results indicated that in addition to negative uncoupling effect, ejection exerts positive effects on ventricular end-systolic pressure that are manifest both quickly and gradually. We hypothesized that the mechanism responsible for the positive effect is length-dependent activation via the larger volume (both at the initiation of contraction and averaged over a cardiac cycle) of a beat that ejects compared to one held isovolumic at end-systolic volume. The results with volume injection were consonant with this concept.

Animals↗
PubMed1992

Isolated ventricular systolic interaction during transient reductions in left ventricular pressure.

The volume and pressure of one ventricle have been demonstrated to modulate the volume and pressure in the contralateral chamber during systole and diastole. To quantitate the isolated systolic effects of left ventricular (LV) pressure on right ventricular (RV) mechanics, we rapidly withdrew blood from the LV immediately after diastole via an apex cannula during a single cardiac cycle in eight open-chest, open-pericardium anesthetized pigs (45 kg) and studied the effects on the RV. Reductions in LV pressure of up to 75 mm Hg were achieved in midsystolic without changing LV or RV diastolic volume or pressure. Resultant changes in RV flow and pressure development during these single unloaded beats may therefore be considered to result from pure systolic interaction. The instantaneous left-to-right systolic pressure gain [G(t)] was determined as the ratio of RV pressure change to LV pressure change as a function of time during systole, and the mean LV-to-RV systolic pressure gain was determined as the ratio of changes in mean systolic RV pressure to changes in mean systolic LV pressure. During LV unloading, there was an average reduction of 62.6 +/- 12.3% in the mean systolic LV pressure, which resulted in decreases of 13.6 +/- 6.4% in mean RV systolic pressure, 17.9 +/- 10.4% in RV stroke volume, and 27.0 +/- 11.3% in RV stroke work. G(t) was found to vary significantly within systole, reaching a minimum of 0.042 +/- 0.014 mm Hg/mm Hg at normalized time 0.70 of the systolic duration and a maximum of 0.079 +/- 0.029 at the end of RV ejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Estimate of the systolic parietal stress of the left ventricle by magnetic resonance imaging. A new approach to the study of the overload].

OBJECTIVE: To determine the systolic parietal stress of the left ventricle by image of magnetic resonance in healthy subjects. MATERIAL AND METHODS: 21 healthy subjects studied: 11 male and 10 female: the ages among 26 and 31 years (29.33). A magnetic resonance of heart was made using the short axis at the level of the papillary muscles, from where the epicardic and endocardic areas of the left ventricular cavity were obtained in diastolic as in systolic by means of the layout with an electronic pencil, later the radius of each drawn up area was calculated, with the value of the radius, the diastolic and systolic thickness was calculated; to obtain the relation between thickness/radio. Once the relation was obtained between thickness/radio in diastole as systole the degree of change between both values and the percentage of this change was calculated. Finally, the systolic parietal stress developed by the left ventricle was calculate with the following formula: S = PVI x A4/A3-A4 x 1.35.PVI: systolic pressure of the left ventricle (the average of 5 synchronized systolic arterial pressures, obtained by an esphingomanometer). A4: endocardic area in systole; A3: epicardial area in systole. The value obtained in this equation was multiplied per 1.35 to turn mmHg gm/cm2. RESULTS: The average of the arterial systolic pressure was of 103.24 +/- 10.27 mmHg; A3 (average 27.58 +/- 2.29); A4 (average 6.84 +/- 0.71); being the systolic stress of the left ventricle of 46.12 +/- 4.9 gm/cm2, not existing significant differences between sexes. CONCLUSIONS: With this new method it is possible to determine with greater exactitude in a noninvasive way, through the best definition of its epicardic and endocardic edges, the areas and the radio of the left ventricular cavity in systole as in diastole, to determine the thickness of the wall and its relation with the radius, for one better valuation of the ventricular function, specially in those subjects with overloads of volume or pressure that depress the ventricular function.

Adult↗
PubMed1982

[Echocardiographic study on systolic left ventricular posterior wall motion in patient with atrial septal defect].

Systolic motion of the left ventricular posterior wall (LVPW) was studied by M-mode and long-axis two-dimensional echocardiography in 35 patients (pts) with secundum type of atrial septal defect (ASD), comparing with that of 19 surgically closed ASD (post ASD), 27 with hypertrophic cardiomyopathy (HCM), 15 with old anteroseptal myocardial infarction (a-s MI) and 28 normal subjects. The results obtained were as follows: 1) Excursion of LVPW (PWE) was significantly increased in the pts with ASD compared with normal subjects (P less than 0.001), but there was no significant difference in PWE between the pts with ASD and the pts with HCM or a-s MI. 2) Mean systolic posterior wall velocity (MPWVs) was significantly decreased in the pts with ASD compared with the pts with HCM (p less than 0.05). However, no significant difference could be found in MPWVs between the pts with ASD and a-s MI or normal subjects. 3) End-systolic thickening of LVPW was significantly increased in the pts with ASD compared with normal subjects (p less than 0.05), the pts with a-s MI (p less than 0.05) and the pts with post ASD (p less than 0.01), except for the pts with HCM. There was a significant difference in % end-systolic thickness of lVPW between the pts with ASD and the pts with a-s MI or post ASD (p less than 0:05). 4) Mid-systolic thickening and % mid-systolic thickening of LVPW were significantly increased in the pts with ASD compared with normal subjects, the pts with a-s MI, the pts with post ASD and the pts with HCM (p less than 0.01). This characteristic mid-systolic bulging of LVPW in the pts with ASD was coincident with early-systolic anterior motion of IVS. 5) Basal portion of LVPW indicated the marked inward contraction during end-systole in 30 of 35 pts (86%) with ASD. In these 30 pts, association of mitral valve (MV) prolapse was observed. 6) Following surgical closure of ASD in 19 pts, MV prolapse disappeared following normalization of excessive endsystolic contraction of the LVPW in 16 pts (functional MV prolapse). In 3 pts, however, posterior MV showed multiple abnormal echoes, indicating MV prolapse or mitral regurgitation (organic MV prolapse). In conclusion, these results suggested that mid-systolic bulging of LVPW in ASD is compensatory reaction for systolic anterior IVS motion, and that mechanism of MV prolapse in ASD is related to abnormal left ventricular geometry due to excessive inward contraction of basal portion of LVPW during end-systole.

Adult↗