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Byline: Ganghong Tian, Bo Xiang, Keith W. Butler, Antonio M. Calafiore, Andrea Mezzetti, Tomas A. Salerno, Roxanne Deslauriers Abstract: This study was designed to assess the effects of intermittent warm blood cardioplegia on myocardial energy metabolites, intracellular pH, and contractile function. The isolated blood-perfused pig hearts were divided into three groups. After 30 minutes of control perfusion, the hearts in group 1 (n = 10) received 90 minutes of continuous warm (37[degrees] C) blood cardioplegia; the hearts in group 2 (n = 9) received six 5-minute periods of warm blood cardioplegia, interrupted by six 10-minute episodes of ischemia (37[degrees] C). The hearts were then reperfused for 30 minutes. The hearts in group 3 underwent 150 minutes of control perfusion without cardioplegia or ischemic episodes. Phosphorus 31-nuclear magnetic resonance spectra showed that a 10-minute interruption of warm blood cardioplegia decreased phosphocreatine levels and intracellular pH by approximately 47% (p < 0.01) and 0.12 unit (p < 0.05), respectively, and increased inorganic phosphate levels by approximately 87%, whereas resumption of cardioplegia for 5 minutes resulted in almost 100% recovery of phosphocreatine and inorganic phosphate levels and intracellular pH. More important, subsequent interruptions did not result in any cumulative changes in phosphocreatine level, inorganic phosphate level, or intracellular pH beyond those changes observed after the initial cardioplegic interruption. Moreover, during reperfusion there were no significant differences in adenosine triphosphate and phosphocreatine levels among the three groups of hearts. Furthermore, hearts from groups 1 and 2 showed comparable recovery of contractile function. These results indicate that six 10-minute interruptions and six 5-minute restorations of warm blood cardioplegia caused only mild and reversible changes in myocardial energy metabolites and intracellular pH and these changes were not cumulative. This study suggests that antegrade intermittent warm blood cardioplegia may provide as much myocardial protection as does antegrade continuous warm blood cardioplegia in the normal heart . (J THORAC CARDIOVASC SURG 1995;109:1155-63) Author Affiliation: Winnipeg, Manitoba, Canada Article History: Received 28 January 1994; Accepted 26 August 1994 Article Note: (footnote) [star] From the Institute for Biodiagnostics,a National Research Council Canada, Winnipeg, Manitoba, Instituto di Clinica Cardiovasculare,b Cattedra di Cardiochirurgia, Ospedale S. Camillo De Chieti, Italy, and the Division of Cardiothoracic Surgery,c St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada., [star][star] Supported by the Medical Research Council of Canada (grant No. 91090P-21383-CEAA-15999)., a Address for reprints: Ganghong Tian, MD, PhD, Institute for Biodiagnostics, National Research Council Canada, 435 Ellice Ave., Winnipeg, Manitoba, Canada R3B 1Y6 (NRC 34755)., aa 0022-5223/95 $3.00 + 0, acents 12/1/60248

A study was conducted to evaluate the role of angiotensin type 1 receptor gene (AGTR1) polymorphism (A1166C) in left ventricular hypertrophy (LVH) mediated by the angiotensin-converting enzyme (ACE) in endurance athletes. The left ventricular mass index (LVMI) was found to be significantly higher in the presence of ACE- DD and AGTR1-AC/CC polymorphisms.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2009.06.007 Byline: Antonio M. Calafiore (a), Angela L. IacA[sup.2] (a), Giovanni Bartoloni (b), Michele Di Mauro (a) Author Affiliation: (a) Department of Cardiac Surgery, University of Catania, Catania, Italy (b) Department of Cardiac Pathology, University of Catania, Catania, Italy Article History: Received 2 May 2009; Accepted 4 June 2009

Antitumor therapy with the anthracycline doxorubicin is limited by a dose-related cardiotoxicity that is aggravated by a concomitant administration of the taxane paclitaxel. Previous limited studies with isolated human heart cytosol showed that paclitaxel was able to stimulate an NADPH-dependent reduction of doxorubicin to its toxic secondary alcohol metabolite doxorubicinol. Here we characterized that 0.25 to 2.5 muM paclitaxel caused allosteric effects that increased doxorubicinol formation in human heart cytosol, whereas 5 to 10 muM paclitaxel decreased doxorubicinol formation. The closely related taxane docetaxel caused similar effects. Basal or taxane-stimulated doxorubicinol formation was blunted by 2,7-difluorospirofluorene-9,5'-imidazolidine-2',4'-dione (AL1576), a specific inhibitor of aldehyde reductases. Doxorubicinol was measured also in the cytosol of human myocardial strips incubated in plasma and exposed to doxorubicin in the absence or presence of paclitaxel or docetaxel and their clinical vehicles Cremophor EL or polysorbate 80. Low concentrations of taxanes stimulated doxorubicinol formation, whereas high concentrations decreased it. Doxorubicinol formation reached its maximum on adding plasma with 6 muM paclitaxel or docetaxel; this corresponded to the partitioning of 1.5 to 2.5 muM taxanes in the cytosol of the strips. Taxane-stimulated doxorubicinol formation was not mediated by vehicles, nor was it caused by increased doxorubicin uptake or de novo protein synthesis; however, doxorubicinol formation was blunted by AL1576. These results show that allosteric interactions with cytoplasmic aldehyde reductases enable paclitaxel or docetaxel to stimulate doxorubicinol formation in human heart. This information serves metabolic insights into the risk of cardiotoxicity induced by doxorubicin-taxane therapies.

Background. The hypothesis that persistence of undivided branches is a common finding after myocardial revascularization using the left internal mammary artery was explored.

We evaluated the effect of ischemia and reperfusion on sarcoplasmic reticulum Ca uptake in patients subjected to cardiac surgery. Our series included 16 patients (seven female, nine male, age 63±2 years): five were subjected to aortic valve replacement, five to aortic and mitral valve replacement, six to coronary artery bypass graft. In each case no clinical, electrocardiographic or echocardiographic evidence of perioperative infarction was observed. Biopsies were obtained from the right atrium of each patient before starting extracorporeal circulation, and after the recovery of spontaneous contractile activity, i.e. after cardioplegia–ischemia–reperfusion. The tissue was homogenized, and oxalate-supported Ca uptake, which represents sarcoplasmic reticulum Ca uptake, was measured in the unfractionated homogenate. The assay was performed under basal conditions and in the presence of 900μmryanodine, in order to block sarcoplasmic reticulum Ca release channels. Under basal conditions at pCa=5.85 the rate of sarcoplasmic reticulum Ca uptake averaged 4.76±0.37 nmol/min per mg of protein in the pre-ischemic samples, and decreased significantly in the post-ischemic samples (3.09±0.29 nmol/min per mg,P<0.01). A significant decrease of Ca uptake after ischemia and reperfusion was observed also in the presence of ryanodine (3.53±0.48 nmol/min per mg) compared to pre-ischemic values (5.98±0.56 nmol/min per mg,P<0.01). Additional experiments showed no change in the Ca sensitivity of Ca uptake in the postischemic samples (KCa=0.48±0.02μm, no significant difference after ischemia and reperfusion). In conclusion, active sarcoplasmic reticulum Ca transport was impaired in human atrial myocardium after reversible ischemia and reperfusion.

The improving results with use of the radial artery and the inferior epigastric artery as coronary bypass conduits were analyzed to assess the suitability of these arteries for myocardial revascularization.

Coronary arteriovenous (AV) fistula is a rare congenital anomaly, mostly diagnosed incidentally during routine coronary angiography. We report a symptomatic patient with right coronary artery to coronary sinus (RCA-CS) fistula, complicated by aneurysmal dilatation and thrombosis of the CS, causing severe mitral regurgitation (MR) and tricuspid regurgitation (TR).

In redo coronary artery bypass grafting a left anterior thoracotomy can be used, if necessary, to avoid a dangerous repeat median sternotomy. In 2 patients with a well-functioning left internal mammary artery graft to a left anterior descending artery attached to the sternum, a radial artery was used with the left subclavian artery as the blood source. This technique can be used successfully in selected cases when a left thoracotomy is advisable and an arterial graft is preferred to a saphenous vein.