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Ventricular Interdependence Heart Failure Patients: Prevalence and Predisposing Conditions
S22 Journal of Cardiac Failure Vol. 12 No. 6 Suppl. 2006 071 Ventricular Interdependence Heart Failure Patients: Prevalence and Predisposing Conditions Benjamin Prentiss, Theo E. Meyer, Michael Stauder; Medicine, University of Massachusetts Memorial Health Care, Worcester, MA; Medicine, Division Cardiology, University of Massachusetts Memorial Health Care, Worcester, MA; Medicine, Division Cardiology, University of Massachusetts Memorial Health Care, Worcester, MA Introduction: The right and left ventricles (RV, LV) share a common septum, and are enclosed in a relatively nondistensible pericardium. Changes in function in the RV can affect that of the LV, and vice versa. This interaction is termed ventricular interdependence (VI) and is characterized by diastolic pressure equilibration. When VI is evident, volume unloading of the RV increases LV diastolic volume and stroke work. Hence, establishing that VI is contributing to the hemodynamic alterations in heart failure becomes an important goal. This study was conducted to: a) establish the relative frequency of VI in patients undergoing hemodynamic evaluation, and b) characterize the conditions that predispose to VI. Methods: Hemodynamic and echocardiographic data were retrospectively analyzed in 526 patients who underwent right and left cardiac catheterization. VI was considered to be present when: a) right atrial (RA) pressures were greater than 18 mmHg and pulmonary occlusion pressures (POC) were # 3 mmHg of the RA pressure. Results: Of the study cohort, 53/529 patients had RA pressures $18 mmHg. The average age of this group was 63 6 13 yrs. The mean RA and POC were 22 6 5 mmHg and 29 6 6 mmHg, respectively. The hemodynamic and echo data of patients with suspected VI (þ) (n 5 34) versus those without (VI-, n 5 19) are shown in the Table. VI is relatively common (64%) when RA pressures are $ 18 mmHg. Only 2/476 patients in the group where the RA !18 mmHg showed right / left pressure equilibration. VI appears less likely in the setting of predominant left-sided chamber dilation and hypokinesis. The prevalence of RV dilation / hypokinesis, MR and TR were similar in the VIþ and VI- groups. Conclusions: VI should be considered to affect hemodynamics in substantial proportion of heart failure patients with RA $ 18 mmHg, and seems more likely to be evident when LV function is relatively preserved. Hemodynamic and Echo data
Age RA (mean mmHg) PA systolic (mmHg) PA diastolic (mmHg) POC (mean, mmHg) RV dilation / HK (n,%) LV dilation / HK (n,%) $ Moderate MR $ Moderate TR
VIþ (n 5 34)
VI (n 5 19)
62 6 15 24 6 6 59 6 14 28 6 7 25 6 6 6 (18%) 11 (32%) 7 (21%) 11 (32%)
64 6 14 20 6 2 59 6 13 28 6 6 32 6 5 6 (33%) 11 (58%) # 4 (21%) 6 (31%)
HK, hypokinesis; MR and TR, mitral and tricuspid regurgitation. P ! 0.05.
#
072 Ventricular Pre-Excitation Acutely Modulates Mechanical Loading Characteristics Following Myocardial Infarction in a Swine Model Allan C. Shuros1, Rodney W. Salo1, Inder S. Anand2; 1Basic Research, Guidant CRM, Saint Paul, MN; 2Cardiology, Veterans Affairs Medical Center, Minneapolis, MN Introduction: Elevated left ventricular (LV) wall stress following myocardial infarction (MI) is associated with subsequent adverse ventricular remodeling. Early activation of this high wall stress region with pacing may provide a method of regionally unloading the heart and attenuating adverse ventricular remodeling chronically. We hypothesized that electrical pre-excitation pacing would acutely modulate regional ventricular contractions in a way that reduces regional wall stress without significantly compromising global hemodynamics. Methods: Apical MI was created in three swine by ligation of the left anterior descending artery. Hemodynamic assessment of cardiac output along with strain measurements from sonomicrometry were recorded 1-week post MI. Atrial tracked (VDD) pacing was used to stimulate the infarct, borderline and/or remote regions of the LV at 4 atrio-ventricular delays (AVD) of 10, 25, 50, and 75% of intrinsic PR interval (IPRI). Lagrangian strain was used as a surrogate assessment of wall stress and the change in wall strain was measured separately in the 3 regions (fig B). Results: Pacing from the border region decreased cardiac output (CO) in a dose-dependent manner with decreasing AVD (fig A). Cardiac output was little affected at the longest AVD (75% IPRI) while at the shortest AVD (10% IPRI), CO was reduced by 23% when compared to no pacing. Pacing from the border region caused a substantial decrease as compared to no pacing in wall strain (fig A). Pacing in the remote region caused a redistribution of strain from the remote to the infarct region (fig B). Overall the greatest benefit in all three regions was seen by pacing in the border zone at 50% AVD (fig. B). Conclusions: As compared to no pacing, pre-excitation pacing caused a substantial decrease in wall strain measured at
1 week post-MI. Overall the greatest effect at reducing wall stress without severely compromising global hemodynamics was seen by pacing in the border zone at 50% AVD.
Age RA (mean mmHg) PA systolic (mmHg) PA diastolic (mmHg) POC (mean, mmHg) RV dilation / HK (n,%) LV dilation / HK (n,%) $ Moderate MR $ Moderate TR
VIþ (n 5 34)
VI (n 5 19)
62 6 15 24 6 6 59 6 14 28 6 7 25 6 6 6 (18%) 11 (32%) 7 (21%) 11 (32%)
64 6 14 20 6 2 59 6 13 28 6 6 32 6 5 6 (33%) 11 (58%) # 4 (21%) 6 (31%)
HK, hypokinesis; MR and TR, mitral and tricuspid regurgitation. P ! 0.05.
#
072 Ventricular Pre-Excitation Acutely Modulates Mechanical Loading Characteristics Following Myocardial Infarction in a Swine Model Allan C. Shuros1, Rodney W. Salo1, Inder S. Anand2; 1Basic Research, Guidant CRM, Saint Paul, MN; 2Cardiology, Veterans Affairs Medical Center, Minneapolis, MN Introduction: Elevated left ventricular (LV) wall stress following myocardial infarction (MI) is associated with subsequent adverse ventricular remodeling. Early activation of this high wall stress region with pacing may provide a method of regionally unloading the heart and attenuating adverse ventricular remodeling chronically. We hypothesized that electrical pre-excitation pacing would acutely modulate regional ventricular contractions in a way that reduces regional wall stress without significantly compromising global hemodynamics. Methods: Apical MI was created in three swine by ligation of the left anterior descending artery. Hemodynamic assessment of cardiac output along with strain measurements from sonomicrometry were recorded 1-week post MI. Atrial tracked (VDD) pacing was used to stimulate the infarct, borderline and/or remote regions of the LV at 4 atrio-ventricular delays (AVD) of 10, 25, 50, and 75% of intrinsic PR interval (IPRI). Lagrangian strain was used as a surrogate assessment of wall stress and the change in wall strain was measured separately in the 3 regions (fig B). Results: Pacing from the border region decreased cardiac output (CO) in a dose-dependent manner with decreasing AVD (fig A). Cardiac output was little affected at the longest AVD (75% IPRI) while at the shortest AVD (10% IPRI), CO was reduced by 23% when compared to no pacing. Pacing from the border region caused a substantial decrease as compared to no pacing in wall strain (fig A). Pacing in the remote region caused a redistribution of strain from the remote to the infarct region (fig B). Overall the greatest benefit in all three regions was seen by pacing in the border zone at 50% AVD (fig. B). Conclusions: As compared to no pacing, pre-excitation pacing caused a substantial decrease in wall strain measured at
1 week post-MI. Overall the greatest effect at reducing wall stress without severely compromising global hemodynamics was seen by pacing in the border zone at 50% AVD.