The Left Ventricle Responds to Acute Graded Elevation of Right Ventricular Afterload by Augmentation of Twist Magnitude and Untwist Rate
ABSTRACT The right and left ventricles share the interventricular septum, which mechanically transmits pressure gradients. The aim of this study was to investigate how acute mild or moderate right ventricular (RV) afterload affects left ventricular (LV) function.
In 14 open-chest pigs (mean weight, 43 ± 4 kg) with preserved pericardium, acute mild (>35 and ≤50 mm Hg) and moderate (>50 and ≤60 mm Hg) RV pressure loading conditions were induced by constriction of the pulmonary artery. Hemodynamic parameters and LV twist and untwist were evaluated under each condition.
From baseline to mild and moderate RV afterload, the mean RV systolic pressure increased from 31.0 ± 4.3 to 41.1 ± 2.7 and 52.7 ± 3.4 mm Hg (P < .001), while LV twist magnitudes increased from 15.4 ± 5.1° to 18.5 ± 3.1° and 19.8 ± 5.0° (P = .004), respectively. Absolute values of LV untwist rate increased from -116.9 ± 64.9°/sec to -160.0 ± 53.3°/sec and -169.1 ± 47.0°/sec, respectively (P = .001). After adjusting for all variables, only the ratio of the early and atrial components of mitral inflow and RV outflow tract acceleration time was significantly associated with the LV twist magnitude and LV untwist rate.
In an acute setting, the left ventricle responds to suddenly elevated RV afterload and decreased RV stroke volume by promptly increasing its twist magnitude and untwist rate.
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ABSTRACT: The haemodynamic effects of acute pulmonary hypertension can be largely attributed to ventricular interdependence during diastole. However, there is evidence that the two ventricles also interact during systole. The aim of the present study was to examine the effects of acute pulmonary hypertension on both components of left ventricular systole, i.e. contraction and relaxation, using load-independent indices. Ten pigs were instrumented with biventricular conductance catheters, a pulmonary artery flow probe and a high-fidelity pulmonary pressure catheter. Haemodynamic measurements were performed in baseline conditions and during stable pulmonary vasoconstriction induced by the thromboxane analogue U46619. Contractility was quantified using the end-systolic pressure-volume and preload recruitable stroke work relationships. The tau-end-systolic pressure relationship was used to assess load-dependency of relaxation. Acute pulmonary hypertension caused a decrease in the slope of the left ventricular preload recruitable stroke work relationship (from 6.64 +/- 1.7 to 5.19 +/- 1.9, mean +/- SD; P < 0.05), a rightward shift of the end-systolic pressure-volume relationship (P < 0.05), and an increase in the slope of the tau-end-systolic pressure relationship (from -0.15 +/- 0.5 to 0.35 +/- 0.17; P < 0.05). The diastolic chamber stiffness constant of both ventricles increased during pulmonary hypertension (P < 0.05). In the present model, acute pulmonary hypertension impairs left ventricular contractile function and relaxing properties. The present study provides additional evidence that, besides the well-known diastolic ventricular cross talk, systolic ventricular interaction may play a significant role in the haemodynamic consequences of acute pulmonary hypertension.European Journal of Anaesthesiology 11/2006; 23(10):824-31. DOI:10.1017/S0265021506000317 · 3.01 Impact Factor
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ABSTRACT: Left ventricular (LV) dimensions and shortening at rest and during treadmill exercise were examined before and after 4 weeks of pulmonary artery (PA) constriction in 6 conscious dogs. The dogs were preinstrumented with LV and right ventricular (RV) catheters, an LV micromanometer, a PA inflatable cuff occluder and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, an apex-base and a free wall segment chord. With PA constriction, RV pressures increased from 49 +/- 4/2 +/- 1 mm Hg (systolic/end-diastolic) to 104 +/- 5/2 +/- 1 at rest and from 71 +/- 9/2 +/- 1 to 133 +/- 8/14 +/- 2 at peak exercise (mean +/- standard error of the mean). Heart rate, LV pressure and LV dP/dt were similar before and after RV pressure overload at rest and with exercise. During exercise at control, systolic shortening increased significantly in all chords. With chronic PA constriction at rest, shortening of all chords also remained normal despite decreases in end-diastolic dimensions, which were most marked in the septal-lateral chord (23% decrease, p less than 0.01). However, during exercise in the presence of RV pressure overload, septal-lateral shortening decreased 46% (p less than 0.01) despite increases in systolic shortening in the other chords similar to the control response. Therefore, although LV function at rest in chronic RV pressure overload is normal, exercise may induce regional abnormalities of LV contraction that appear to be mediated by a reduced contribution of the ventricular septum to LV ejection.The American Journal of Cardiology 05/1984; 53(8):1187-93. DOI:10.1016/0002-9149(84)90660-X · 3.43 Impact Factor
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ABSTRACT: This study sought to characterize the early features of diabetic cardiomyopathy by magnetic resonance imaging (MRI) tagging. The earliest manifestations of diabetic cardiomyopathy have not been well established, especially under tight glycemic management. We hypothesized that torsion measurements would identify subclinical contractile alterations in type I diabetics with normal left ventricular ejection fraction, mass, blood pressure, and aggressive glycemic control. We also sought to characterize the influence of elevated resting heart rates (HRs) of diabetics on torsion. Sixteen patients with type I diabetes and 10 control patients underwent cine and tagged MRI with a 1.5-T scanner. Torsion, strain, and their rates were measured. To quantify the influence of chronotropic and inotropic stimulation on torsion, nine healthy volunteers underwent MRI tagging at rest, after atropine injection, and after exercise. Diabetic patients (hemoglobin A1c, 6.8 +/- 0.4%) had a higher resting HR (77.0 +/- 12.4 beats/min vs. 59.0 +/- 5.6 beats/min; p < 0.01), higher maximal torsion by 23% (3.5 +/- 0.9 degrees/cm vs. 2.7 +/- 0.4 degrees/cm; p < 0.01) and higher maximal systolic torsion rate (TR-s) by 25% (0.013 +/- 0.003 degrees/cm/s vs. 0.010 +/- 0.002 degrees/cm/s, p = 0.01). Torsion did not significantly change with chronotropic stimulation (p = 0.30). In diabetics under tight glycemic control, we observed a surprising increase in torsion and TR-s unrelated to chronotropic influences of HR. We propose that increased torsion and TR-s could represent early predictive markers of the propensity to cardiac dysfunction in asymptomatic type I diabetics. Furthermore, these findings seem fundamental to the diabetic state itself and unaccounted for by other comorbidities.Journal of the American College of Cardiology 02/2006; 47(2):384-90. DOI:10.1016/j.jacc.2005.08.061 · 15.34 Impact Factor