Decrease In Left Ventricular Stroke Volume Research Articles

Abstract 17334: Effects of Alcohol Consumption on Fiver-Year Change in Cardiac Structure and Function: In the Echocardiographic Study of Latinos

Background: The relationship between alcohol consumption and clinical heart failure has been extensively studied. There have been little longitudinal data documenting alcohol effects on cardiac structure and function in a community-based population. Methods: The second Echocardiographic Study of Latinos (ECHO-SOL2) was designed to provide echocardiographic parameters that characterized longitudinal cardiac structure and function in a random and representative sample of 1,818 participants ≥45 years old. Participants underwent to serial echocardiograms at 2011-2014 (exam 1) and ~5-6 years later at 2016-2019 (exam 2). Quantification of alcohol was created on a gender-specific basis. Multiple linear regression models were adjusted for age and sex. Results: The mean age at enrollment was 56.4 years old, 57% were women. At baseline, impaired left ventricular (LV) systolic function and increased right ventricular (RV) function were associated with binge drinkers (P = 0.01). At 5-6 years later, heavy drinkers had a significant decrease in LV ejection fraction (P = 0.01). Moderate and binge drinkers demonstrated worsening diastolic function over time (P ≤ 0.01). Binge drinkers demonstrated a progressive decrease in LV mass index (P = 0.02), decrease in LV stroke volume (P = 0.01) and further reduction in RV function (P < 0.01). Conclusion: Alcohol consumption was associated with longitudinal changes in cardiac structure and function, mostly among binge drinkers, which can lead to impaired myocardial contractility compared to nondrinkers.

Serelaxin Improves Regional Myocardial Function in Experimental Heart Failure: An In Vivo Cardiac Magnetic Resonance Study.

BackgroundAnimal studies demonstrated that serelaxin lessens fibrosis in heart failure. This study assessed its effect on myocardial deformation using cardiac magnetic resonance and elucidated its relationship to gene regulation and histology in a mouse heart failure model.Methods and ResultsC57BL/6J mice were subjected to SHAM (n=4) or transverse aortic constriction (TAC). At week 10, TAC mice were randomized to receive either serelaxin (0.5 mg/kg per day; n=11) or vehicle (n=13) for 4 weeks. Cardiac magnetic resonance imaging was performed at baseline and repeated at the end of the study (week 14). Cine images were used to calculate left ventricular (LV) global longitudinal, circumferential, and radial strain. Hearts were examined for histology and gene expression. Compared with SHAM, mice 10 weeks after TAC showed increased LV mass with significant decreases in LV deformation parameters, indicating subclinical deterioration of myocardial function. At week 14, TAC mice given serelaxin demonstrated significant improvements in all LV strain parameters and no decrease in LV stroke volume and ejection fraction compared with TAC mice given vehicle. A significant positive correlation between global circumferential strain and the extent of myocardial fibrosis was found, and global circumferential strain correlated significantly with the expression of heart failure genes in serelaxin‐treated mice.ConclusionsSerelaxin improved cardiac magnetic resonance–derived myocardial deformation parameters as well as histomorphometric and gene expression findings in mice with heart failure. Cardiac magnetic resonance–derived myocardial mechanics correlate with histology and gene expression, stressing its utilization in myocardial remodeling.

Pre-Load–Induced Changes in Forward LV Stroke and Functional Mitral Regurgitation: Echocardiographic Detection of the Descending Limb of Starling's Curve

ObjectivesThe purpose of this study was to clarify the prognostic significance of diagnosing whether the failing heart is functioning on the descending limb of the Starling curve by using echocardiography with passive leg lifting (PLL). BackgroundPatients with advanced heart failure can shift to the descending limb of the Starling curve, in which pre-load does not lead to an expected increase in forward left ventricular stroke volume (LVSV). MethodsThirty-five consecutive patients with left ventricular (LV) ejection fraction of <40% underwent echocardiography at rest during baseline and during PLL to increase pre-load. ResultsDespite PLL, a paradoxical decrease in forward LVSV was observed in 15 (43%) patients. Changes in forward LVSV inversely correlated with those in functional mitral regurgitation (r = −0.56). The primary endpoint of cardiac death or hospitalization due to worsening heart failure occurred in 15 (43%) patients during follow-up (2.8 ± 2.2 years). There were a number of significant predictors of the primary endpoint in the univariate Cox analysis: baseline E/A ratio (p = 0.0002), paradoxical decrease in LVSV despite PLL (hazard ratio: 4.44; 95% confidence interval: 1.41 to 14.0; p = 0.011), baseline LV end-systolic volume (p = 0.023), and baseline LV ejection fraction (p = 0.034). In the bivariate Cox analysis, an addition of the paradoxical decrease in LVSV significantly enhanced the predictive power of all other univariate predictors. ConclusionsHeart failure patients with LV systolic dysfunction on the descending limb of the Starling curve can be recognized by the paradoxical decrease in LVSV despite PLL, and the prognostic predicting power is additive to the other traditional echocardiographic predictors. Also, our results suggest that functional mitral regurgitation is an important reason for the descending limb of the Starling curve, which is clinically recognized as the pre-load–induced decrease in forward LVSV.

Clinical Manifestations and Diagnosis of Right Ventricular Failure

Right ventricular (RV) failure is a complex clinical syndrome characterized by impaired RV filling and ejection. RV function is altered in the setting of either pressure overload or volume overload. RV failure may result from a primary reduction of myocardial contractility caused by ischemia, cardiomyopathy, or arrhythmia, but left ventricular (LV) failure remains the leading cause. As RV dysfunction progresses to RV failure, the RV chamber becomes more spherical and tricuspid regurgitation is aggravated, leading to increasing venous congestion. Ventricular interdependence may result in impaired LV filling, a decrease in LV stroke volume, and low cardiac output. The important clinical manifestations of RV failure are fluid retention, decreased systolic reserve, low cardiac output, or arrhythmias. The initial diagnosis is based on clinical history and physical examination. A chest X-ray, electrocardiogram, and biochemical tests should be routinely obtained to evaluate the underlying causes and comorbidities. Bedside echocardiography provides valuable information on cardiac structure and function. RV ejection fraction is the most commonly used index of RV function although it is a highly load-dependent index. (Korean J Med 2016;91:131-138)

Role of Variations in Pulmonary and Cardiac Hemodynamics in the Reduction of the Venous Return during Experimental Ischemia of the Left Ventricular Myocardium

During left-ventricular myocardial ischemia, the decrease in the venous return is determined by reduction of cardiac output, which results from heart rate deceleration and decrease in left-ventricular stroke volume. The latter is related to a decrease in myocardial contractility and blood storage in the pulmonary circuit. Blood accumulation in the lungs is not observed during stimulation of the vagus nerve or treatment with propranolol (against the background of the same values of the negative chronotropic and inotropic effects as during myocardial ischemia). The left-ventricular stroke volume increases, while the cardiac output and venous return decrease to a lesser extent under these conditions.

Diastolic ventricular interactions in endurance-trained athletes during orthostatic stress

Enhanced left-ventricular (LV) compliance is a common adaptation to endurance training. This adaptation may have differential effects under conditions of altered venous return. The purpose of this investigation was to assess the effect of cardiac (un)loading on right ventricular (RV) cavity dimensions and LV volumes in endurance-trained athletes and normally active males. Eight endurance-trained (Vo(2max), 65.4 +/- 5.7 ml.kg(-1).min(-1)) and eight normally active (Vo(2max), 45.1 +/- 6.0 ml.kg(-1).min(-1)) males underwent assessments of the following: 1) Vo(2max), 2) orthostatic tolerance, and 3) cardiac responses to lower-body positive (0-60 mmHg) and negative (0 to -80 mmHg) pressures with echocardiography. In response to negative pressures, echocardiographic analysis revealed a similar decrease in RV end-diastolic cavity area in both groups (e.g., at -80 mmHg: normals, 21.4%; athletes, 20.8%) but a greater decrease in LV end-diastolic volume in endurance-trained athletes (e.g., at -80 mmHg: normals, 32.3%; athletes, 44.4%; P < 0.05). Endurance-trained athletes also had significantly greater decreases in LV stroke volume during lower-body negative pressure. During positive pressures, endurance-trained athletes showed larger increases in LV end-diastolic volume (e.g., at +60 mmHg; normals, 14.1%; athletes, 26.8%) and LV stroke volume, despite similar responses in RV end-diastolic cavity area (e.g., at +60 mmHg: normals, 18.2%; athletes, 24.2%; P < 0.05). This investigation revealed that in response to cardiac (un)loading similar changes in RV cavity area occur in endurance-trained and normally active individuals despite a differential response in the left ventricle. These differences may be the result of alterations in RV influence on the left ventricle and/or intrinsic ventricular compliance.

Cardiac Function During Intraperitoneal CO2 Insufflation for Aortic Surgery: A Transesophageal Echocardiographic Study

The effect of laparoscopy on cardiac function is controversial. We hypothesized that cardiac dysfunction related to increased afterload could be predominant in patients undergoing elective abdominal aortic repair. To test this hypothesis, we conducted a transesophageal echocardiographic study in 15 patients during laparoscopic aortic surgery. We systematically assessed left ventricular (LV) and right ventricular (RV) functions. Measurements were obtained in the supine position without pneumoperitoneum and with an intraabdominal pressure of 14 mm Hg. Then, patients were turned to the right lateral position without pneumoperitoneum and intraabdominal pressure was increased to 7 mm Hg and to 14 mm Hg. Pneumoperitoneum induced a 25% arterial blood pressure increase and a 38% increase in LV systolic wall stress. A 25% decrease in LV ejection fraction and an 18% decrease in LV stroke volume were observed, associated with an increase in LV end-systolic volume. LV diastolic function impairment was observed without change in LV end-diastolic volume. Respiratory alterations in superior vena cava diameter were never observed, suggesting that volume status remained optimal. Respiratory changes in RV stroke volume were increased according to intraabdominal pressure and body position, reflecting an increase in RV afterload. In conclusion, peritoneal CO2 insufflation in patients scheduled for laparoscopic aortic surgery could impair LV and RV systolic functions as a consequence of increased afterload.

Stroke volume and cardiac output decrease at termination of obstructive apneas.

Patients with obstructive sleep apnea (OSA) experience repetitive nocturnal oscillations of systemic arterial pressure that occur in association with changes in respiration and changes in sleep state. To investigate cardiac function during the cycle of obstruction (apnea) and resumption of ventilation (recovery), we continuously measured left ventricular stroke volume (LVSV) and mean arterial blood pressure (MAP) during non-rapid-eye-movement sleep in six males with severe OSA (apnea/hypopnea index > or = 30 events/h associated with oxygen saturation < 82%). LVSV was assessed continuously using an ambulatory ventricular function monitor (VEST; Capintec). The apnea-recovery cycle was divided into three phases: 1) early apnea (EA), 2) late apnea (LA), and 3) recovery (Rec). In all subjects recovery was associated with an abrupt decrease in LVSV [54.0 +/- 14.5 (SD) ml] compared with either EA (91.4 +/- 14.7 ml; P < 0.001) or LA (77.1 +/- 15.2 ml; P < 0.005). Although heart rate increased with recovery, the increase was not sufficient to compensate for the decrease in LVSV so that cardiac output (CO) fell (EA: 6,247 +/- 739 ml/min; LA: 5,741 +/- 1,094 ml/min; Rec: 4,601 +/- 1,249 ml/min; EA vs. Rec, P < 0.01; LA vs. Rec, P < 0.025). Recovery was also associated with a significant increase in MAP. We speculate that such abrupt decreases in LVSV and CO at apnea termination, occurring coincident with the nadir of oxygen saturation, may further compromise tissue oxygen delivery.

Influence of pleural pressure variations on cardiovascular system dynamics: a model study.

A mathematical model of the human cardiovascular system (CVS) is used to study the effect of different respiratory manoeuvres on the circulation. The model simulates the normal CVS and the interaction between the heart and the intrathoracic pressure. The vascular system is represented by resistive, capacitive and inertial elements whereas the ventricles are assumed to function according to the time-varying elastance concept based on their transmural pressures. The model predicts that normal inspiratory effeort effects an increase in the venous return, an increase in the pulmonary flow and a slight decrease in the left ventricular stroke volume (LVSV), which represents a decrease in ejection due to the increased LV transmural pressure. A step decrease in pleural pressure to −40 mm Hg, representing the Muller manoeuvre (MM), accentuates these findings, showing a decrease in LVSV in spite of an increase in the LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV) and the LV filling pressure, expressed as the mean left atrial transmural pressure. Simulating intermittent positive pressure ventilation (IPPV) with added positive end expiratory pressure (PEEP) shows an 18·6 per cent decrease in the cardiac output compared with quiet respiration. The calculated results of the model are in good agreement with available experimental data, suggesting that most of these findings may be explained by basic haemodynamic principles in the uncontrolled CVS.

Transient analysis of cardiopulmonary interactions. II. Systolic events.

The etiology of the fall in left ventricular stroke volume (LVSV) and arterial pressure with a negative intrathoracic pressure (NITP) during inspiration is controversial. An increase in LV afterload produced by NITP has been proposed as one explanation but is difficult to evaluate if preload is also altered. To test the hypothesis that a systolic event alone, i.e., a change in LV afterload or contractility, can reduce LVSV during inspiration independent of changes in LV preload, a rapid transient NITP confined to systole was produced by electrocardiogram-triggered phrenic nerve stimulation in eight anesthetized dogs. Intrathoracic descending aortic diameters were measured by sonomicrometry to transduce qualitative changes in aortic transmural pressure. With the airway completely obstructed systolic NITP resulted in a decrease in LVSV (-8.1%, P less than 0.001) but an increase in the systolic anteroposterior (0.54 mm, P less than 0.01) and right-to-left (0.45 mm, P less than 0.01) aortic diameters compared with preceding beat. Similar significant changes were observed with the airway unobstructed. These observations are consistent with an increased afterload imposed on the LV reducing LVSV and egress of blood out of the thorax. Prolonging NITP to include both systole and diastole, a profound fall in LVSV is observed, consistent with the independent influences of systolic and diastolic events combining to diminish LVSV.(ABSTRACT TRUNCATED AT 250 WORDS)

A model of the effects of respiration on left ventricular performance

We have investigated the interaction of left ventricular afterload and right-heart volume on left ventricular performance. By utilizing a right-heart bypassed heart-lung preparation, we have been able to control independently each factor. We have previously suggested that the major influences of the inspiratory decrease in pleural pressure in decreasing left ventricular stroke volume (LVSV) may be via the inspiratory increases in left-heart afterload and right-heart volume (RHV). Thus, our preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Our results show that increases in transmural (relative to pleural pressure) aortic pressure (Pao) caused an increased left ventricular end-diastolic pressure (LVEDP), and that the effect of equivalent increases in Pao was greater when RHV was greater. Increase in RHV had minimal effects at low volume, but resulted in large increases in LVEDP at large RHV. These effects were markedly attenuated after pericardiectomy. Rapid increases in either RHV or Pao produced transient falls in LVSV. Our results are consistent with the hypothesis that increases in both right-heart volume and LV afterload contribute to the inspiratory decrease in LVSV and increase in LVEDP.