Long-term Outcomes and Anticoagulation in Mitral Valve Surgery-A Report From The Society of Thoracic Surgeons Database.

BACKGROUND: Anticoagulation after bioprosthetic mitral valve (MV) replacement (BMVR) and repair (MVrep) is controversial. We explore outcomes among BMVR and MVrep patients in The Society of Thoracic Surgeons Adult Cardiac Surgery Database based on discharge anticoagulation status. METHODS: BMVR and MVrep patients aged ≥65 years in The Society of Thoracic Surgeons Adult Cardiac Surgery Database were linked to the Centers for Medicare and Medicaid Services claims database. Long-term mortality, ischemic stroke, bleeding, and a composite of the primary end points were compared as a function of anticoagulation. Hazard ratios (HRs) were calculated using multivariable Cox regression. RESULTS: A total of 26,199 BMVR and MVrep patients were linked to the Centers for Medicare and Medicaid Services database; of these, 44%, 4%, and 52% were discharged on warfarin, non-vitamin K-dependent anticoagulant (NOAC), and no anticoagulation (no-AC; reference), respectively. Warfarin was associated with increased bleeding in the overall study cohort (HR, 1.38; 95% CI 1.26-1.52) and in the BMVR (HR, 1.32; 95% CI, 1.13-1.55) and MVrep subcohorts (HR, 1.42; 95% CI, 1.26-1.60). Warfarin was associated with decreased mortality only among BMVR patients (HR, 0.87; 95% CI, 0.79-0.96). Stroke and the composite outcome did not differ across cohorts with warfarin. NOAC use was associated with increased mortality (HR, 1.33; 95% CI 1.11-1.59), bleeding (HR, 1.37; 95% CI, 1.07-1.74), and the composite outcome (HR, 1.26; 95% CI, 1.08-1.47). CONCLUSIONS: Anticoagulation was used in fewer than half of mitral valve operations. In MVrep patients, warfarin was associated with increased bleeding and was not protective against stroke or mortality. In BMVR patients, warfarin was associated with a modest survival benefit, increased bleeding, and equivalent stroke risk. NOAC was associated with increased adverse outcomes.

Pseudoprolapse of the anterior leaflet in chronic ischemic mitral regurgitation: identification and repair.

OBJECTIVE: Recurrence rates as high as 30% have been observed 6 months after treatment of chronic ischemic mitral regurgitation (CIMR) with isolated annuloplasty. We postulated that the high early recurrence rates resulted from the presence of untreated pseudoprolapse of the anterior leaflet. METHODS: We conducted a retrospective study of all mitral valve repairs for CIMR performed by a single surgeon (S.W.H.) from 1995 to 2011. After annuloplasty, Gore-Tex neochordae were added if the high-pressure saline test indicated the presence of pseudoprolapse of the anterior leaflet. RESULTS: A total of 47 patients underwent mitral valve repair for CIMR. Of the 47 patients, 24 (51%) were found to have pseudoprolapse requiring the addition of neochordae. For all patients, the average age was 65.1 years, and 65.2% were men. Fourteen (30%) had had a preoperative intra-aortic balloon pump placed by cardiologists. Fourteen (30%) had severe pulmonary hypertension. Concomitant coronary artery bypass grafting was performed in 40 patients, with an average of 2.2 grafts; 7 had previously undergone coronary artery bypass grafting. Mitral Carpentier-Edwards physio annuloplasty rings were used in all patients with a mean size of 29 mm. One patient died postoperatively. Follow-up data were available for all 47 patients at an average of 4.9 years. The 5-year survival rate was 82.5%. The mean pre- and postoperative New York Heart Association class, ejection fraction, and mitral regurgitation grade were 3 and 1.52 (P < .0001), 34% and 41% (P = .0006), and 3.51 and 1.08 (P < .0001), respectively. Two patients developed greater than moderate mitral regurgitation. CONCLUSIONS: Effective repair of CIMR should include surgical techniques to correct pseudoprolapse of the anterior leaflet, when present. The selective addition of Gore-Tex neochordae to an undersized annuloplasty nearly eliminates recurrent regurgitation after mitral valve repair for CIMR.

Pulmonary artery agenesis and Kommerell's diverticulum presenting with hemoptysis.

Unilateral pulmonary artery agenesis is a rare congenital anomaly that is commonly associated with additional cardiovascular abnormalities. We report a case of intrapulmonary hemorrhage and hemoptysis in a patient with left-sided pulmonary artery agenesis as well as the first description of this anomaly in a patient with a diverticulum of Kommerell. The patient was successfully treated by performing a left pneumonectomy.

Age- and gender-related differences in mitochondrial oxygen consumption and calcium with cardioplegia and diazoxide.

BACKGROUND: We have recently shown that the cardioprotection afforded by cardioplegia is affected by age and gender and is less effective in the aged female rabbit heart compared with the aged male rabbit heart. We hypothesized that these differences were due to age and gender-specific modulation of mitochondrial oxygen consumption and mitochondrial free matrix calcium ([Ca2+](Mito)) content occurring during early reperfusion. METHODS: To test this hypothesis, 104 male and female rabbit hearts, mature (15 to 20 weeks) and aged (>32 months), were subjected to Langendorff perfusion. Control hearts were perfused for 75 minutes. Global ischemia hearts were underwent 30 minutes of equilibrium, 30 minutes of global ischemia, and 15 minutes of reperfusion. Cardioplegia (potassium/magnesium) +/- diazoxide was infused 5 minutes before global ischemia. Mitochondria were isolated from left ventricular tissue and used for the measurement of oxygen consumption and [Ca2+](Mito). RESULTS: Mitochondrial oxygen consumption was significantly increased in the mature and aged female hearts in all treatment groups (p < 0.001 versus male). Cardioplegia +/- diazoxide modulated mitochondrial oxygen consumption, but these effects were significantly decreased in the aged heart and in the female heart (p < 0.001 each versus male). Cardioplegia (potassium/magnesium) significantly decreased [Ca2+](Mito) (p < 0.001 versus global ischemia) in aged but not mature hearts. The addition of diazoxide to potassium/magnesium significantly decreased [Ca2+](Mito) in mature and aged males (p < 0.001 versus potassium/magnesium) but not in females. CONCLUSIONS: These results demonstrate that mitochondrial oxygen consumption and [Ca2+](Mito) are modulated by age and gender and play an important role in the differences observed between mature and aged male and female response to global ischemia and the cardioprotection afforded by cardioplegia +/- diazoxide.

Age- and gender-related differences in ischemia/reperfusion injury and cardioprotection: effects of diazoxide.

BACKGROUND: Recent studies have demonstrated that aging is associated with reduced tolerance to ischemia and that the aged (not senescent) female heart has greater susceptibility to ischemia as compared with the aged male heart. Previously, we have shown that ischemia can be modulated with cardioplegia in the male heart; however, efficacy in the female heart was unknown. METHODS: In this study, male and female mature (15 to 20 weeks) aged (>32 months) rabbit hearts (n = 134) were subjected to Langendorff perfusion. Control hearts were perfused for 180 minutes. Global ischemia hearts received 30 minutes of equilibrium, 30 minutes of global ischemia, and 120 minutes of reperfusion. Cardioplegia +/- diazoxide was infused separately, 5 minutes before global ischemia. RESULTS: Global ischemia significantly decreased postischemic functional recovery and significantly increased infarct size in the mature and aged male and female heart (p < 0.05 versus control). The effects of global ischemia were significantly exacerbated (p < 0.05) in the aged heart as compared with the mature heart. Cardioplegia +/- diazoxide significantly increased postischemic functional recovery and significantly decreased infarct size in mature male and female hearts, but these effects were significantly decreased in the aged heart (p < 0.05) and in the aged female as compared with the aged male heart. CONCLUSIONS: Postischemic functional recovery and infarct size are affected by age but not by gender. The cardioprotection afforded by cardioplegia is affected by age and gender with a strong age-by-gender interaction for end-diastolic pressure and infarct size. Our results indicate that currently optimized cardioplegia protocols effective in the male heart are not as efficacious in the aged female heart.

Opening of mitochondrial KATP channels enhances cardioprotection through the modulation of mitochondrial matrix volume, calcium accumulation, and respiration.

Previously, we have shown that the pharmacological opening of the mitochondrial ATP-sensitive K channels with diazoxide (DZX) enhances the cardioprotection afforded by magnesium-supplemented potassium (K/Mg) cardioplegia. To determine the mechanisms involved in the cardioprotection afforded by K/Mg + DZX cardioplegia, rabbit hearts (n=24) were subjected to isolated Langendorff perfusion. Control hearts were perfused for 75 min. Global ischemia (GI) hearts were subjected to 30 min of equilibrium, 30 min of GI, and 15 min of reperfusion. K/Mg and K/Mg + DZX cardioplegia hearts received either K/Mg or K/Mg + DZX for 5 min before GI and reperfusion. Tissue was harvested for mitochondrial isolation and transmission electron microscopy (TEM). Mitochondrial structure, area, matrix volume, free calcium, and oxygen consumption were determined. TEM demonstrated that GI mitochondria were damaged and that K/Mg and K/Mg + DZX preserved mitochondrial structure. TEM and light scattering demonstrated separately that mitochondrial matrix and cristae area and matrix volume were significantly increased after GI and reperfusion with GI > K/Mg + DZX > K/Mg hearts (P <0.05 vs. control). Mitochondrial free calcium was significantly increased in GI and K/Mg hearts. K/Mg + DZX significantly decreased mitochondrial free calcium accumulation (P <0.05 vs. GI and K/Mg). State 3 oxygen consumption and respiratory control index in malate (complex I substrate)- and succinate (complex II substrate)-energized mitochondria were significantly decreased (P <0.05 vs. control) in the GI and K/Mg + DZX groups. These data indicate that the enhanced cardioprotection afforded by K/Mg + DZX cardioplegia occurs through the preservation of mitochondrial structure and the significant decrease in mitochondrial free calcium accumulation and mitochondrial state 3 oxygen consumption.