Preservation of myocardial function by mechanical circulatory support during prolonged ischaemia

The effect of mechanical circulatory support on left ventricular (LV) function was evaluated during prolonged myocardial ischaemia. Regional wall thickening of a normal and an ischaemic LV region were determined in eight calves (mean body weight 76 kg) using pairs of ultrasonic crystals. LV end-diastolic (mmHg) and peak systolic (mmHg) pressure as well as maximum dP/dt (mmHg s−) were calculated from LV high-fidelity pressure tracings. The left circumflex coronary artery was ligated proximally for 6 h and reperfused for 18 h. Circulatory support by the assist device was performed from the beginning of ischaemia to the end of the experiment. After a mean time of 4 h all animals showed ventricular fibrillation, which was converted successfully in six animals after a mean time interval of 5 h. Five animals survived after 24 h. The non-surviving animals had larger infarcts, greater creatine kinase release and a larger drop in cardiac output during ischaemia. Haemodynamic measurements were carried out after turning off the assist device. Inotropic stimulation with 0-68 mg . min− dopamine i. v. was performed at the end of the study. LV regional function showed systolic bulging during myocardial ischaemia. After 18 h of reperfusion, the ischaemic wall recovered and showed normal systolic wall thickening in the presence of an increased LV preload. LV relaxation was prolonged after reperfusion, suggesting diastolic dysfunction. It is concluded that mechanical circulatory support is effective in protecting myocardial function during prolonged ischaemia in approximately two-thirds of the animals, despite severe ischaemic ventricular dysfunction and intermittent ventricular fibrillatio

Left ventricular volume determination in dogs: a comparison between conductance technique and angiocardiography

Left ventricular (LV) volume was determined simultaneously by monoplane cineangiocardiography and conductivity using a multielectrode conductance catheter at rest and during pressure loading in seven mongrel dogs (mean body weight 22 kg). LV volumes were calculated frame-by-frame (75 frames s−1) by angiocardiography and matched with instantaneous volumes obtained by conductivity. There was an excellent correlation between the two techniques at rest (correlation coefficient, r = 0.96) and during pressure loading (r = 0.92) when the data of each dog were pooled. The standard error of estimate of the mean angiographic volume was 4%. The slope of the regression analysis showed a small but significant (P <0.01) decrease from 0.365 at rest to 0.289 during pressure loading, whereas the intercept remained unchanged (24 versus 26 ml). Since no calibration for parallel conductivity of the surrounding tissue was performed, LV end-systolic volume was significantly over- and LV ejection fraction significantly underestimated whereas LV end-diastolic volume was estimated correctly by the conductance technique. It is concluded that LV end-diastolic volume can be determined accurately by the conductance technique in dogs. However, LV end-systolic volume is significantly over- and ejection fraction significantly under-estimated. Since there is a good correlation between angiocardiography and conductivity, exact determination Of LV volumes and ejection fraction is feasible using a correction factor. The change is slope of the regression equation between angiocardiography and conductivity suggests a change in conductivity of the surrounding tissue during pressure loading which limits the application of the conductance catheter to stable haemodynamic situations or calls for repeated calibrations by an independent technique during acute intervention

Regional diastolic dysfunction in postischaemic myocardium in calf: effect of nisoldipine

Objective: The aim was to assess the effect of nisoldipine on left ventricular systolic and diastolic function during prolonged myocardial ischaemia. Methods: The left circumflex coronary artery was ligated for 2 h and reperfused for 4 h in 12 calves. The animals were randomised to a control group (n=6) or to treatment with 1.25 mg·h−1 intravenous nisoldipine (n=6) during 2 h of ischaemia. Circulatory support by a ventricular assist device was performed throughout the experiment except for the time of haemodynamic measurements. Regional wall thickening of a normal and an ischaemic left ventricular region was determined using pairs of ultrasonic crystals. Left ventricular pressure was measured by micromanometry. Left ventricular wall thickness and regional wall stiffness at a common preload of 10 mm Hg were calculated using an elastic model with shifting asymptote. Results: Ten animals survived after 6 h. No difference was observed in systolic function between controls and nisoldipine treated animals. Systolic thickening of the ischaemic wall remained depressed 4 h after reperfusion and showed some recovery after dopamine infusion. Ischaemic wall stiffness at a common preload was lower after nisoldipine during ischaemia and reperfusion than in controls. Control wall stiffness remained unchanged during the whole experiment with and without nisoldipine. Diastolic thinning of the ischaemic wall was prevented by nisoldipine during ischaemia and after reperfusion. Conclusions: Prolonged myocardial ischaemia is associated with increased myocardial stiffness of the ischaemic wall. Mechanical unloading can help to bridge the acute phase but cannot prevent postischaemic diastolic dysfunction of the ischaemic wall. Nisoldipine has a beneficial effect on regional diastolic function during ischaemia and reperfusion by decreasing regional wall stiffness and preventing diastolic thinning of the ischaemic wall. Cardiovascular Research 1993;27:531-53

Preservation of myocardial function by mechanical circulatory support during prolonged ischaemia.

The effect of mechanical circulatory support on left ventricular (LV) function was evaluated during prolonged myocardial ischaemia. Regional wall thickening of a normal and an ischaemic LV region were determined in eight calves (mean body weight 76 kg) using pairs of ultrasonic crystals. LV end-diastolic (mmHg) and peak systolic (mmHg) pressure as well as maximum dP/dt (mmHg s-1) were calculated from LV high-fidelity pressure tracings. The left circumflex coronary artery was ligated proximally for 6 h and reperfused for 18 h. Circulatory support by the assist device was performed from the beginning of ischaemia to the end of the experiment. After a mean time of 4 h all animals showed ventricular fibrillation, which was converted successfully in six animals after a mean time interval of 5 h. Five animals survived after 24 h. The non-surviving animals had larger infarcts, greater creatine kinase release and a larger drop in cardiac output during ischaemia. Haemodynamic measurements were carried out after turning off the assist device. Inotropic stimulation with 0.68 mg.min-1 dopamine i.v. was performed at the end of the study. LV regional function showed systolic bulging during myocardial ischaemia. After 18 h of reperfusion, the ischaemic wall recovered and showed normal systolic wall thickening in the presence of an increased LV preload. LV relaxation was prolonged after reperfusion, suggesting diastolic dysfunction. It is concluded that mechanical circulatory support is effective in protecting myocardial function during prolonged ischaemia in approximately two-thirds of the animals, despite severe ischaemic ventricular dysfunction and intermittent ventricular fibrillation

Left ventricular volume determination in dogs: a comparison between conductance technique and angiocardiography

Left ventricular (LV) volume was determined simultaneously by monoplane cineangiocardiography and conductivity using a multielectrode conductance catheter at rest and during pressure loading in seven mongrel dogs (mean body weight 22 kg). LV volumes were calculated frame-by-frame (75 frames s−1) by angiocardiography and matched with instantaneous volumes obtained by conductivity. There was an excellent correlation between the two techniques at rest (correlation coefficient, r = 0.96) and during pressure loading (r = 0.92) when the data of each dog were pooled. The standard error of estimate of the mean angiographic volume was 4%. The slope of the regression analysis showed a small but significant (P <0.01) decrease from 0.365 at rest to 0.289 during pressure loading, whereas the intercept remained unchanged (24 versus 26 ml). Since no calibration for parallel conductivity of the surrounding tissue was performed, LV end-systolic volume was significantly over- and LV ejection fraction significantly underestimated whereas LV end-diastolic volume was estimated correctly by the conductance technique. It is concluded that LV end-diastolic volume can be determined accurately by the conductance technique in dogs. However, LV end-systolic volume is significantly over- and ejection fraction significantly under-estimated. Since there is a good correlation between angiocardiography and conductivity, exact determination Of LV volumes and ejection fraction is feasible using a correction factor. The change is slope of the regression equation between angiocardiography and conductivity suggests a change in conductivity of the surrounding tissue during pressure loading which limits the application of the conductance catheter to stable haemodynamic situations or calls for repeated calibrations by an independent technique during acute intervention

Regional diastolic dysfunction in postischaemic myocardium in calf: effect of nisoldipine

OBJECTIVE: The aim was to assess the effect of nisoldipine on left ventricular systolic and diastolic function during prolonged myocardial ischaemia. METHODS: The left circumflex coronary artery was ligated for 2 h and reperfused for 4 h in 12 calves. The animals were randomised to a control group (n = 6) or to treatment with 1.25 mg.h-1 intravenous nisoldipine (n = 6) during 2 h of ischaemia. Circulatory support by a ventricular assist device was performed throughout the experiment except for the time of haemodynamic measurements. Regional wall thickening of a normal and an ischaemic left ventricular region was determined using pairs of ultrasonic crystals. Left ventricular pressure was measured by micromanometry. Left ventricular wall thickness and regional wall stiffness at a common preload of 10 mm Hg were calculated using an elastic model with shifting asymptote. RESULTS: Ten animals survived after 6 h. No difference was observed in systolic function between controls and nisoldipine treated animals. Systolic thickening of the ischaemic wall remained depressed 4 h after reperfusion and showed some recovery after dopamine infusion. Ischaemic wall stiffness at a common preload was lower after nisoldipine during ischaemia and reperfusion than in controls. Control wall stiffness remained unchanged during the whole experiment with and without nisoldipine. Diastolic thinning of the ischaemic wall was prevented by nisoldipine during ischaemia and after reperfusion. CONCLUSIONS: Prolonged myocardial ischaemia is associated with increased myocardial stiffness of the ischaemic wall. Mechanical unloading can help to bridge the acute phase but cannot prevent postischaemic diastolic dysfunction of the ischaemic wall. Nisoldipine has a beneficial effect on regional diastolic function during ischaemia and reperfusion by decreasing regional wall stiffness and preventing diastolic thinning of the ischaemic wall