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Objective: Cardioplegic arrest remains the method of choice for myocardial protection in cardiac surgery. Poly(adenosine 5 0 -diphosphateribose) synthetase (PARS) inhibitor has been suggested to attenuate the ischemia-reperfusion injury in myocardial infarction by preventing energy depletion associated with oxidative stress. We investigated the efficacy of a cardioplegic solution containing a PARS inhibitor, 3-aminobenzamide (3-AB), for myocardial protection against ischemia-reperfusion injury caused by cardioplegic arrest. Methods: Isolated hearts were set on a Langendorff apparatus and perfused. The hearts were arrested for 90 min with a cardioplegic solution given at 30-min intervals and then reperfused for 20 min. The hearts of rat in the 3-AB(2) group ðn ¼ 8Þ were perfused with a standard cardioplegic solution and terminal warm cardoplegia, whereas the 3-AB(þ) group ðn ¼ 8Þ received these solutions supplemented with 3-AB (100 mM). Left ventricular function and release of cardiac enzymes were monitored before and after cardioplegic arrest. After reperfusion, NAD þ (nicotinamide-adenine dinucleotide) levels were assessed, and the tissues were examined immunohistochemically for oxidative stress and apoptosis. Results: During reperfusion, the 3-AB(þ ) group showed significantly higher ðP ¼ 0:005Þ dp=dt and lower creatine phosphokinase (CPK) level and glucotamic-oxaloacetic transaminase (GOT) in the effluent (CPK; P ¼ 0:003; GOT; P , 0:001Þ: The cardiomyocytes of the 3-AB(þ) group also preserved a higher NAD þ level ðP , 0:001Þ: Immunohistochemical study of oxidative stress revealed a lesser extent ðP ¼ 0:007Þ of nuclear staining and a lower fraction of apoptosis in the 3-AB(þ) group. Conclusion: Cardioplegic solution supplemented with 3-AB provides efficient myocardial protection in cardioplegic ischemic reperfusion by suppressing oxidative stress and overactivation of PARS. q 2004 Published by Elsevier B.V.

Undersized mitral annuloplasty (MAP) is effective in patients with dilated cardiomyopathy and functional mitral regurgitation (MR) since, as well as addressing the MR, the MAP may also reshape the dilated left ventricular (LV) base. However, the direct benefits of this possible reshaping on LV function in the absence of underlying MR remain incompletely understood. The study aim was to identify these benefits in a canine model of acute heart failure.Six dogs underwent MAP with a prosthetic band on the posterior mitral annulus, using four mattress sutures. The sutures were passed individually through four tourniquets and exteriorized untied via the left atriotomy. Sonomicrometry crystals were implanted around the mitral annulus and left ventricle to measure geometry and regional function. Acute heart failure was induced by propranolol and volume loading after weaning from cardiopulmonary bypass; an absence of MR was confirmed by echocardiography. MAP was accomplished by cinching the tourniquets. Data were acquired at baseline, after induction of acute heart failure, and after MAP.MAP decreased mitral annular dimensions in both commissure-commissure and septal-lateral directions. Concomitantly, the diastolic diameter of the LV base and LV sphericity decreased (i.e., improved) from 37.4 +/- 9.3 to 35.9 +/- 10 mm (p = 0.063), and from 67.9 +/- 18.6% to 65.3 +/- 18.9% (p = 0.016), respectively. Decreases were evident in both LV end-diastolic pressure (from 17 +/- 7 to 15 +/- 6 mmHg, p = 0.0480 and Tau (from 48 +/- 8 to 45 +/- 8 ms, p0.01), while fractional shortening at the LV base increased from 7.7 +/- 4.5% to 9.4 +/- 4.5% (p = 0.045). After MAP, increases were identified in both cardiac output (from 1.54 +/- 0.57 to 1.65 +/- 0.57 1/min) and Emax (from 1.86 +/- 0.9 to 2.41 +/- 1.31 mmHg/ml).The data acquired suggest that isolated MAP may have certain benefits on LV dimension/function in acute heart failure, even in the absence of MR. However, further investigations are warranted in a model of chronic heart failure.

Background— Left ventricular aneurysm repair (LVR) reduces LV wall stress and improves LV function. However, as we reported previously, the initial improvement of LVR was short-term because of LV remodeling but could be maintained longer with postoperative use of an angiotensin-converting enzyme (ACE) inhibitor. Atrial natriuretic peptide (ANP) has been used to treat patients with heart failure by natriuretic and vasodilatory actions. Recent reports have suggested that ANP inhibits the rennin-angiotensin system. In this study, the effects of ANP after LVR were evaluated. Methods and Results— Rats that had an LV aneurysm 4 weeks after left anterior descending artery ligation underwent LVR by plicating the LV aneurysm and were randomized into 2 groups: LVR+A group was intravenously administrated with 10 μg/h of carperitide, recombinant α-hANP, by osmotic-pump for 4 weeks, and the LVR group was given normal saline. Echocardiography revealed better LV remodeling and function in LVR+A group than in LVR group. Four weeks after LVR, left ventricular end diastolic pressure (LVEDP) and Tau were significantly lower in LVR+A group (LVEDP: 10±4 in LVR+A group versus 18±6 mm Hg in LVR group, Tau: 13±2 versus 17±2ms). End-systolic elastance (Ees) was higher in LVR+A group (Ees: 0.34±0.2 versus 0.19±0.11 mm Hg/μL). The levels of myocardial ACE activity in LVR+A group was significantly lower than in LVR group. The mRNA expressions of brain natriuretic peptide and transforming growth factor β1 inducing fibrosis significantly decreased in LV myocardium in LVR+A group. Histologically, myocardial fibrosis was significantly reduced in LVR+A group. Conclusions— Intravenous administration of ANP had beneficial effects on LV remodeling, function, and fibrosis after LVR. ANP could be a useful intravenous infusion drug for postoperative management after LV repair surgery.

The Batista operation for dilated cardiomyopathy (DCM) has not, thus far, yielded satisfactory results. One of the explanations for disappointing results is the absence of a suitable animal model of dilated cardiomyopathy. Scientific research on volume reduction surgery needs to be carried out in an appropriate experimental model. This chapter reviews the few studies of volume reduction surgery using animal models of DCM published thus far, including our studies.

Objective: Volume reduction surgery for dilated cardiomyopathy has not yielded predictable outcomes. The purpose of this study was to clarify the efficacy of modified volume reduction surgery in preserving the left ventricular apex and reducing the left ventricular diameter at the base to maintain fiber continuity. Methods: Heart failure was induced with propranolol in 12 dogs, and the animals were randomized into 2 groups. In one group the left ventricular wall was plicated between the 2 papillary muscles from the middle to the apex (apex-sacrificing volume reduction surgery, group A, n=6), and in the other group plication was done from the base to the middle (apex-sparing volume reduction surgery, group B, n=6). Left ventricular function was then compared between the groups by using echocardiography and sonomicrometry crystals. Results: After volume reduction surgery, the fractional area change at the base in group B was greater than that in group A (40% ± 3% vs 27% ± 4%, P =.003). Cardiac output in group B was better than that in group A (2.5 ± 0.2 vs 1.8 ± 0.2 L/min, P =.023). Left ventricular end-diastolic pressure in group A was higher than that in group B (16 ± 2 vs 8 ± 1 mm Hg, P =.001). Fractional shortening in the long axis, as assessed by means of sonomicrometry, was better in group B than in group A. Conclusions: Apex-sparing volume reduction surgery capable of maintaining left ventricular fiber continuity provided better left ventricular function in both the systolic and diastolic phases than apex-sacrificing volume reduction surgery in the acute heart failure model. This modification might improve the results of left ventricular volume reduction surgery. J Thorac Cardiovasc Surg 2003;125:669-77