Coronary artery bypass grafting versus percutaneous coronary intervention in single-vessel left anterior descending artery disease: mid-term propensity matching study.

Introduction: Coronary artery bypass grafting (CABG) has been considered to be the proven therapeutic choice for coronary artery disease. However, percutaneous coronary intervention (PCI) with drug-eluting stents is increasingly used for extensive coronary artery disease with contradictory results. The aim of this study is to compare immediate- and mid-term results of CABG where skeletonized internal mammary artery (IMA) was used as in situ graft versus PCI with serolimus drug eluted stents (SES) in single-vessel left anterior descending artery (LAD) disease. Methods: In 2014-2022, 938 patients treated for isolated LAD revascularization were included in this study. Among them, there were 346 patients with CABG-IMA and 592 patients with SES-PCI. CABG-IMA patients (n = 266) were compared with SES-PCI patients (n = 266) in propensity score-matched method.Primary outcome measures were identified as all-cause mortality at 30 days and 3 years after surgery, while secondary outcome measures were length of hospital stay and the incidence of postoperative major adverse cardiovascular and cerebrovascular events (MACCE). Results: Increased incidence for post procedural MACCE after PCI was recorded (CABG = 1.2% vs. PCI = 5.3%; p < 0.05). There was no difference in immediate-term (30 days: CABG = 1.2% vs. PCI = 1.5%; p = ns) and mid-term (3 years: CABG = 3.7% vs. PCI = 4.5%; p = ns) mortality between the groups. Patient after SES-PCI had shorter length of hospital stay (CABG = 7.7 days vs. PCI = 3.8 days; p < 0.05). Conclusion: The results of the study indicated that CABG-IMA performed at the time of myocardial revascularization in single-vessel LAD disease is better than SES-PCI. Our conclusion is independent of traditionally accepted risk factors incorporated in the Logistic EuroSCORE II (European System for Cardiac Operative Risk Evaluation) and SYNTAX score II (Synergy Between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery Score II) and is exclusively method related.

Clipless skeletonized internal mammary artery harvesting with harmonic technology.

Since the introduction of the mammary artery harvesting procedure, electrocautery has been used as a standard method of care. However, mammary artery spasm, subadventitial haematoma and mammary artery damage due to clips dispositioning or high thermal energy injury have been recorded. To achieve a perfect mammary artery graft, we propose the usage of a high-frequency ultrasound device, usually recognized as a harmonic scalpel. It reduces thermal-related injuries, the use of clips and the risk of mammary artery spasm and/or dissection.

Himalayan P wave in a patient admitted for cardiac surgery.

Giant or Himalayan P waves are tall and peaked, the most prominent in lead II, and generally indicate enlargement of the right atrium. It has been rarely seen in clinical practice. The mechanism of Himalayan P wave formation is most likely related with prolonged conduction of electrical impulses through the enlarged right atrium. We describe the case of a patient with Himalayan P wave admitted for cardiac surgery.

High-energy drinks may provoke aortic dissection.

High-energy drinks have become extremely popular after Red Bull's promotion at 1987 in Austria and 1997 in the United States. Since then, we witnessed spectacular increase in different brands, caffeine content and market consumption all over the world. However, there are no reports published in the scientific literature related with detrimental side effects after heavy consumption of high-energy drinks. We report a series of three high-risk cardiovascular patients who had aortic dissection (De Bakey type I and II) following significant consumption of high-energy drinks. All of them required emergency surgical procedure and were remaining stable after surgery. We propose that uncontrolled consumption of high-energy drinks, especially in patients with underlying heart disease, could provoke potentially lethal cardiovascular events as well as acute aortic dissection.

Systematic reductive annuloplasty of the mitral and tricuspid valves in patients with end-stage ischemic dilated cardiomyopathy.

OBJECTIVE: Patients with ischemic dilated cardiomyopathy exhibit extensive remodeling of the left ventricle, annular dilation, and significant mitral and tricuspid regurgitation. These changes increase per operative morbidity and mortality, and emphasize patient candidacy for heart transplantation. The aim of this study is to show immediate and long-term results after reductive annuloplasty of double (mitral and tricuspid) orifices, performed at the time of coronary artery bypass grafting, as an alternative to heart transplantation. METHODS: There were 226 consecutive patients (205 males, 21 females) with ischemic dilated cardiomyopathy, mean ejection fraction below 30% [(26.6 +/- 3.1)%], and mean left ventricle end-diastolic internal diameter greater than 7.0 cm (7.3 +/- 0.3 cm). In addition to myocardial revascularization, Carpentier's mitral annuloplasty and posterior semicircular reductive annuloplasty were performed in 37 and 189 patients, respectively. In all 226 patients, a modified De Vega's tricuspid annuloplasty was performed. RESULTS: Postoperative 30-day mortality was 7.5% (17 patients). Survival rates after 5 and 10 years were (61.5 +/- 4.0)% and (38.05 +/- 8.0)%, respectively. CONCLUSION: Reductive annuloplasty of mitral and tricuspid orifices performed at the time of myocardial revascularization could be beneficial in selective patients with ischemic dilated cardiomyopathy. Results indicate that this method should not be recognized as a valve repair, but ventricular repair procedure also.

Adenosine attenuates C-terminal but not N-terminal proteolysis of cTnI during cardioplegic arrest.

BACKGROUND: Specific site proteolysis and loss of troponin I (TnI) during myocardial ischemic events can contribute to myocardial dysfunction. Adenosine supplementation of cardioplegic solutions results in improved functional preservation of the heart. We investigated the effect of adenosine on N-terminal and C-terminal proteolysis of TnI in the heart. MATERIALS AND METHODS: Hearts from male Sprague-Dawley rats were isolated and perfused at a constant pressure. Cardioplegic arrest (St. Thomas #2 +/- 100 microm adenosine) was induced and hearts frozen at various times during the arrest. Antibodies directed against specific regions of TnI were used to visualize TnI in whole heart homogentates, as well as from cellular fractions, using western blot analysis. RESULTS: Cardioplegic arrest alone resulted in early N-terminal proteolysis of TnI, followed by later loss of sequences from the C-terminal end of the molecule. In addition, secondary protein bands that were immunoreactive to amino acid sequences centrally located on the TnI molecule were observed. There was also evidence of dissociation of TnI from the other myofibrillar proteins. The supplementation of cardioplegic solution with adenosine significantly attenuated the late C-terminal proteolytic degradation of TnI and its apparent dissociation from myofibrils proteins but had no effect on the early N-terminal proteolysis associated with cardioplegic arrest. CONCLUSIONS: These data may provide an explanation for partial protection against postarrest myocardial dysfunction provided by adenosine.

Prostacyclin reduces incidence of myocardial damage after coronary endarterectomy.

BACKGROUND: After coronary endarterectomy, patients have an increased incidence of perioperative myocardial infarction. This study was undertaken to evaluate the possible reduction of perioperative myocardial damage after coronary endarterectomy by intravenous utilization of prostacyclin. METHODS: Elective coronary artery bypass grafting was performed in 1,190 patients with diffuse and distal coronary artery disease, in whom endarterectomy of one or more vessels was used as a treatment. All procedures were done with cardiopulmonary bypass. There were 584 patients in the prostacyclin-treated group, and 606 patients in the control group. Prostacyclin (10 ng x kg(-1) x min(-1)) was started 20 minutes before the cross-clamp removal, or at the time of rewarming, and was continued during the first 24 hours after surgery. The incidence of perioperative myocardial damage was detected by creatine kinase-MB enzyme measurement, and electrocardiographic and left ventricular function changes. RESULTS: A significant decrease in perioperative myocardial damage was detected in the group treated with prostacyclin with respect to the control group. CONCLUSIONS: Prostacyclin infusion initiated during revascularization and continued in the early postoperative course could be successfully employed for the prevention of thrombocyte aggregation and potentially decrease the overall incidence of significant myocardial damage after coronary endarterectomy.

Subcellular distribution of protein kinase C isozymes during cardioplegic arrest.

BACKGROUND: On the basis of the hypothesis that cardioplegia-associated myocardial depression was due to activation of protein kinase C, we examined whether specific protein kinase C isozymes would translocate to a cellular fraction containing myofilaments. METHODS: Isolated rat hearts were perfused with Krebs-Ringer bicarbonate buffer for 30 minutes and arrested with 4 degrees C St Thomas No. 2 cardioplegic solution for 0 to 120 minutes (n = 5 per group). The 3 fractions of the left ventricle tissue represented the myofibrillar/nuclear fraction (P1), membranes (P2), and cytosol (supernatant). The distributions of protein kinase C isozymes alpha, delta, epsilon, and eta were examined after separation by electrophoresis, immunoblotting/chemiluminescence, and densitometry. RESULTS: A significant increase in protein kinase C-delta in the P1 fraction was detected after 5 minutes of cardioplegic arrest and remained increased for 60 minutes. Increases in P1 protein kinase C-alpha and -epsilon were seen transiently at 5 minutes, and protein kinase C-epsilon demonstrated a secondary increase in P1 at 30 to 60 minutes. There was also a significant relative increase in protein kinase C-alpha and protein kinase C-delta in the P2 fraction after 60 minutes of cardioplegia. CONCLUSIONS: These data are consistent with our hypothesis that activation of protein kinase C isozymes is associated with altered myofilament function after cardioplegic arrest.

Comparison of adenosine, isoflurane, and desflurane on myocardial tissue oxygen pressure during coronary artery constriction in dogs.

OBJECTIVE: To compare adenosine-, isoflurane-, or desflurane-induced hypotension with and without left anterior descending (LAD) coronary artery constriction for the effects on myocardial tissue oxygen pressure (PmO(2)) in dogs. DESIGN: Prospective, randomized, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred dogs (n = 18). INTERVENTIONS: Dogs were anesthetized with 1.5% isoflurane (n = 12) or 8% desflurane (n = 6). A flow probe and balloon occluder were placed on the LAD artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial minus coronary sinus oxygen content. MEASURES AND MAIN RESULTS: Measures were made during hypotension produced by adenosine infusion, 2.8% isoflurane, or 14% desflurane with and without LAD constriction to decrease blood flow 30%. Without LAD artery constriction, adenosine infusion increased LAD flow 90% and MVO(2) 70%, 2.8% isoflurane produced no change in MVO(2), and 14% desflurane decreased MVO(2) 25%, but no treatment changed PmO(2). LAD artery constriction decreased PmO(2) 50% by itself. Adenosine infusion during LAD constriction decreased tissue oxygen pressure an additional 60%, 2.8% isoflurane produced no change, and 14% desflurane increased PmO(2) 100%. CONCLUSION: There was an inverse relationship between the effect of adenosine, 2.8% isoflurane, and 14% desflurane on MVO(2) and PmO(2) during ischemia. This is consistent with reports that increasing oxygen demand worsens myocardial ischemia.

Sodium nitroprusside-induced, but not desflurane-induced, hypotension decreases myocardial tissue oxygenation in dogs anesthetized with 8% desflurane.

OBJECTIVE: To compare sodium nitroprusside (SNP)-induced hypotension with desflurane-induced hypotension for the effects on myocardial blood flow and tissue oxygenation in dogs. DESIGN: Prospective, randomized, crossover, nonblinded. SETTING: University teaching hospital. PARTICIPANTS: Male nonpurpose-bred hounds (n = 8). INTERVENTIONS: Dogs were anesthetized with 8% desflurane. Catheters were inserted into the femoral artery and coronary sinus. A flow probe was placed in the left anterior descending (LAD) branch of the coronary artery. A sensor that measured myocardial oxygen pressure (PmO(2)) was inserted into the myocardium of the left ventricle. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial - coronary sinus oxygen content. MEASUREMENTS AND MAIN RESULTS: Measurements were made at baseline blood pressure levels of 99 mmHg (measure 1), during hypotension to 62 to 66 mmHg using intravenous SNP or 14% desflurane (measure 2), and during SNP or 14% desflurane with blood pressure support using phenylephrine (measure 3). Each dog randomly received both hypotensive treatments, separated by 1 hour. Baseline measures were PmO(2) = 46 +/- 9 mmHg, LAD flow = 43 +/- 11 mL/min, and MVO(2) = 2.47 +/- 0.73 mL O(2)/min. During hypotension induced with SNP, PmO(2) decreased 30% (p < 0.05), LAD flow increased 40% (p < 0.05), and MVO(2) did not change. During hypotension induced with 14% desflurane, PmO(2) did not change, and LAD flow and MVO(2) decreased 25% and 40% (p < 0.05). Blood pressure support with phenylephrine increased LAD flow and MVO(2) but did not change PmO(2) during SNP or 14% desflurane treatment. CONCLUSION: SNP-induced hypotension produced myocardial vasodilation, but tissue oxygenation was impaired. PmO(2) was maintained during desflurane-induced hypotension.

Inhibiting adenosine deaminase modulates the systemic inflammatory response syndrome in endotoxemia and sepsis.

By pharmacological manipulation of endogenous adenosine, using chemically distinct methods, we tested the hypothesis that endogenous adenosine tempers proinflammatory cytokine responses and oxyradical-mediated tissue damage during endotoxemia and sepsis. Rats were pretreated with varying doses of pentostatin (PNT; adenosine deaminase inhibitor) or 8-sulfophenyltheophylline (8-SPT; adenosine receptor antagonist) and then received either E. coli endotoxin (lipopolysaccharide; 0.01 or 2.0 mg/kg) or a slurry of cecal matter in 5% dextrose in water (200 mg/kg). Resultant levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-10 were measured in serum and in liver and spleen. Untreated, 2 mg/kg lipopolysaccharide elevated serum TNF-alpha, IL-1beta, and IL-10. PNT dose dependently attenuated, without ablating, the elevation in serum TNF-alpha and IL-1beta and raised liver and spleen IL-10. PNT also attenuated elevation of TNF-alpha in serum, liver, and spleen at 4 and 24 h after sepsis induction, and 8-SPT resulted in higher proinflammatory cytokines. Modulating endogenous adenosine was also effective in exacerbated (8-SPT) or diminished (PNT) tissue peroxidation. Survival from sepsis was also improved when PNT was used as a posttreatment. These data indicate that endogenous adenosine is an important modulatory component of systemic inflammatory response syndromes. These data also indicate that inhibition of adenosine deaminase may be a novel and viable therapeutic approach to managing the systemic inflammatory response syndrome without ablating important physiological functions.

Reductive annuloplasty of double orifices in patients with primary dilated cardiomyopathy.

BACKGROUND: Patients with primary dilated cardiomyopathy exhibit extensive remodeling of the left ventricle, mitral and tricuspid annular dilation and both mitral and tricuspid regurgitation. These factors significantly contribute to heart failure, and are predictors of early lethal outcome. The aim of this study is to show hemodynamic and clinical improvement after reductive annuloplasty of both mitral and tricuspid orifices in primary dilated cardiomyopathy. METHODS: There were 76 patients with primary dilated cardiomyopathy. Mitral annuloplasty using a Carpentier-Edwards sizer was performed on 9 patients, and posterior semicircular reductive annuloplasty was performed on 67 patients. Modified De Vega's tricuspid annuloplasty was performed on all patients. RESULTS: Immediate and long-term results showed significant improvement in hemodynamic values and myocardial contractility after operation. CONCLUSIONS: Reductive annuloplasty of both mitral and tricuspid orifices corrects remodeling of the left ventricle of the heart, changes sphericity and geometry of the left ventricle, improves hemodynamic action of the left and right ventricle, and slows down progression of heart failure. We recommend reductive annuloplasty of both mitral and tricuspid orifices before or soon after the first decompensation.