Risk factors for re-exploration due to bleeding after coronary artery bypass grafting.

OBJECTIVE: The study aimed to investigate relevant clinical risk factors for re-exploration due to bleeding after primary coronary artery bypass graft (CABG) surgery, and to evaluate the influence of antiplatelet and antifibrinolytic drugs. DESIGN: Three retrospective analyses were performed on patients who underwent CABG: (1) Logistic regression was used to identify clinical risk factors for re-exploration (n = 3000). (2) A case-control study (n = 228) was used to obtain information on exposure of antithrombotic and hemostatic therapy. (3) Based on exposure to antiplatelet and antifibrinolytic therapy, and odds ratios (ORs) in multivariate logistic models, the proportion of re-explorations attributed to these drugs was calculated. RESULTS: A receiver operating characteristic curve was created for clinical risk factors. The C-index was 0.64, indicating limited ability to predict re-exploration for bleeding. Clopidogrel was the only drug influencing the risk of re-exploration (OR 3.2, 95% CI 1.7-5.9). The harmful effect of clopidogrel was confirmed in multivariate model (OR 4.7, 95% CI 2.2-9.9), and aprotinin had a protective effect of the same magnitude (OR 0.2, 95% CI 0.1-0.6). CONCLUSIONS: Clopidogrel is an essential risk factor for re-exploration due to bleeding, and attributable to at least one-quarter of surveyed cases. Aside from pharmaceuticals, there are no strong clinical risk factors.

Severe chronic aortic regurgitation after percutaneous coronary intervention: a case report and literature review.

BACKGROUND: Severe aortic regurgitation (AR) is an extremely rare complication after coronary catheterization and percutaneous coronary intervention (PCI), where most reported cases have required relatively urgent surgical intervention due to acute-onset AR and cardiac decompensation. CASE SUMMARY: We report a case of a 60-year-old woman that previously presented with a non-ST-elevation myocardial infarction (NSTEMI) due to an ostial right coronary artery stenosis. During the course of 2 years, she developed five recurrent NSTEMI due to in-stent thrombosis, necessitating either a new coronary stent or balloon. She developed a chronic severe AR due to a drug-eluting coronary stent protruding from the right coronary artery and underwent successful aortic valve replacement and coronary artery by-pass grafting. DISCUSSION: We performed a literature review and identified 16 reported cases of iatrogenic severe aortic regurgitation related to coronary catheterization or percutaneous coronary intervention. All patients developed an acute aortic regurgitation and, thus, we report the first case of a delayed complication caused by a protruding coronary stent. The surgical strategy is related to the extent of the damage, where smaller perforations or lacerations seems to be feasible for aortic valve repair and larger defects more often lead to aortic valve replacement. Our patient developed a fibrotic right coronary cusp which could not be used to perform a successful aortic valve repair.

Quadruple Bioprosthetic Valve Replacement in a Patient With Severe Carcinoid Heart Disease.

Carcinoid heart disease typically affects the tricuspid and pulmonary valves, causing severe regurgitation and/or stenosis. Valve surgery has been shown to reduce right heart failure and improve long-term prognosis in these patients. We report a severe case of a patient with all 4 heart valves involved who underwent successful quadruple bioprosthetic valve replacement. (Level of Difficulty: Intermediate.).

Re-exploration for bleeding associated with increased incidence of the need for reintervention after coronary artery bypass graft surgery.

OBJECTIVES: Re-exploration for bleeding after cardiac surgery increases the risk of other severe postoperative complications and early mortality. Patients re-explored for bleeding after coronary artery bypass grafting are potentially subject to threats to graft patency. Our goal was to assess the effects of re-exploration for bleeding regarding the incidence of coronary angiographies, the need for coronary reintervention and mortality during long-term follow-up. METHODS: Within the SWEDEHEART registry, all isolated coronary artery bypass operations with a single internal mammary artery and saphenous vein graft in patients aged 40-80 between the years 2005 and 2015 were identified. Incidences of coronary angiography and the subsequent need for coronary reintervention were recorded, and multivariable adjusted hazard ratios (HRs) were calculated. RESULTS: The study cohort consisted of 27 957 patients, and the mean follow-up time was 6.5 ± 3.1 years. The incidence of re-exploration for bleeding was 3.8% (n = 1071). The cumulative incidence [95% confidence interval (CI)] of a clinically occurring coronary angiography within 1 year after surgery was 7.8% (6.3-9.7) in re-explored and 4.8% (4.6-5.1) in non-re-explored patients, and the adjusted HR was 1.64 (1.31-2.06), (P < 0.001). The cumulative incidence of the need for coronary reintervention within 1 year (95% CI) was 4.9% (3.7-6.4) in re-explored and 2.6% (2.4-2.8) in non-re-explored patients, and the adjusted HR was 1.91 (1.43-2.56). No difference in incidence or hazard ratio was observed beyond the first year. Mortality rate was increased within but not beyond 90 days after surgery. CONCLUSIONS: Re-exploration for bleeding is associated with an increased risk for the need of repeat coronary reintervention during the first year after coronary artery bypass surgery.

Higher Preoperative Plasma Thrombin Potential in Patients Undergoing Surgery for Aortic Stenosis Compared to Surgery for Stable Coronary Artery Disease.

Aortic stenosis (AS) and coronary artery disease (CAD) influence the coagulation system, potentially affecting hemostasis during cardiac surgery. Our aim was to evaluate 2 preoperative global hemostasis assays, plasma thrombin potential and thromboelastometry, in patients with severe aortic valve stenosis compared to patients with CAD. A secondary aim was to test whether the assays were associated with postoperative bleeding. Calibrated automated thrombogram (CAT) in platelet-poor plasma and rotational thromboelastometry (ROTEM) in whole blood were analyzed in patients scheduled for elective surgery due to severe AS (n = 103) and stable CAD (n = 68). Patients with AS displayed higher plasma thrombin potential, both thrombin peak with median 252 nmol/L (interquartile range 187-319) and endogenous thrombin potential (ETP) with median 1552 nmol/L/min (interquartile range 1340-1838), when compared to patients with CAD where thrombin peak was median 174 nmol/L (interquartile range 147-229) and ETP median 1247 nmol/L/min (interquartile range 1034-1448; both P < .001). Differences persisted after adjustment for age, gender, comorbidity, and antithrombotic treatment. Differences observed in thromboelastometry between the groups did not persist after adjustment for baseline characteristics. Bleeding amount showed no relationship with plasma thrombin potential but weakly to thromboelastometry ( R2 = .064, P = .001). Patients with AS exhibited preoperatively increased plasma thrombin potential compared to patients with CAD. Plasma thrombin potential was not predictive for postoperative bleeding in patients scheduled for elective surgery.

The platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment.

INTRODUCTION: Addition of clopidogrel to patients treated with ASA has been shown to decrease the incidence of in-stent thrombosis after percutaneous coronary interventions. However, it has also been reported that up to 30% of patients do not achieve adequate platelet inhibition from standard dosages of ASA and clopidogrel. There is a demand for reliable methods to measure the individual platelet inhibiting effect of this combination therapy. MATERIALS AND METHODS: The primary aim of the present investigation was to compare three methods for evaluation of the platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment. Thirty patients presenting for coronary angiography/PCI were included. Two patients were excluded due to technical problems. All patients were on 75-100 mg ASA/day for at least 8 days. Blood samples were analysed before and 16 h after a 300 mg clopidogrel bolus dose. The platelet inhibiting effect was measured with (1) Whole blood flow cytometry (17 patients); (2) a bed-side test, Platelet Mapping assay for the thrombelastograph (28 patients); and (3) PFA (Platelet function analyser) -100 (26 patients). RESULTS: With flow cytometry, the percentage of platelets expressing P-selectin (p=0.03) on their surface decreased significantly after the bolus dose of clopidogrel. There was also a reduction of platelets binding fibrinogen when stimulated with ADP. A significantly (p=0.002) increased platelet inhibition could also be demonstrated with Platelet Mapping. PFA-100 could not measure any significant platelet inhibiting effect of clopidogrel. CONCLUSION: A significant platelet inhibition could be demonstrated with flow cytometry and the Platelet Mapping assay, but not with PFA-100. However, levels of response for the individual patient with these three methods were inconsistent. Further studies are needed to evaluate how the results correlate to the clinical risk of thrombosis and bleeding.

Central hemodynamics during lung recruitment maneuvers at hypovolemia, normovolemia and hypervolemia. A study by echocardiography and continuous pulmonary artery flow measurements in lung-injured pigs.

OBJECTIVE: The impact of lung-recruitment maneuvers on heart function at different volemic levels has not been studied in detail. We therefore investigated the effect on central hemodynamics of lung recruitment maneuvers at hypovolemia, normovolemia and hypervolemia in experimental lung injury. DESIGN: Randomized, controlled, cross-over experimental study. SETTING: Animal laboratory at a university hospital. PARTICIPANTS: Eleven anesthetized and lung-lavaged pigs. INTERVENTION: The animals were randomized to 10-s lung recruitment maneuvers followed by 30-s maneuvers (40 cm H(2)O airway pressure) or vice versa, performed under hypovolemia, normovolemia and hypervolemia. MEASUREMENTS AND MAIN RESULTS: Left-ventricular end-diastolic diameter and cardiac output were measured before, during, and 1 min and 5 min after the lung recruitment maneuver and left-ventricular eccentricity index was calculated for before and during the maneuver. Cardiac output and left-ventricular end-diastolic diameter (within parentheses) decreased significantly during both the 10-s and 30-s lung recruitment maneuvers at hypovolemia, by a mean of 89% (35) and 92% (33), at normovolemia by 75% (33) and 86% (32), and at hypervolemia by 56% (32) and 64% (43), respectively. At hypovolemia, cardiac output was increased above baseline 1-5 min following the 30-s maneuver. Left-ventricular eccentricity index increased significantly during the maneuver, indicating right ventricular dysfunction. CONCLUSIONS: In this animal lung injury model, lung recruitment maneuvers significantly decreased left-ventricular end-diastolic volume and cardiac output at hypovolemia. Hypervolemia did partly counteract this compromise. In addition, a marked right-ventricular dysfunction during the maneuver was found.

Dissecting ventricular pseudoaneurysm after perimyocarditis-a case report.

BACKGROUND: The current case describes the fast development of a pseudoaneurysm in a patient that presented with signs of systemic inflammation and generally deranged blood work. CASE PRESENTATION: The pseudoaneurysm appeared within one week of disease onset. The anatomic extent of the pseudoaneurysm was unusual, as it dissected intramurally beneath the septum, inferior to the right ventricle and had effect on the RV filling. The etiology could not be definitely defined, since in adults the most common cause for pseudoaneurysm development is recent myocardial infarction, but in this patient the coronary arteries were healthy. Instead it could have been a consequence of an aggressive perimyocarditis. CONCLUSIONS: Due to the unpredictable nature of pseudoaneurysms we advocate early contact with a center with cardiothoracic surgery expertise for rapid surgical intervention.

Causes of mortality with ticagrelor compared with clopidogrel in acute coronary syndromes.

OBJECTIVE: To describe specific causes of death and evaluate whether bleeding events and infection contributed to mortality in all ticagrelor-treated and clopidogrel-treated patients with acute coronary syndromes. METHODS: In the PLATelet inhibition and patient Outcomes (PLATO) trial, ticagrelor significantly reduced rates of vascular and total death compared with clopidogrel. In the 905 patients who died postenrolment in the PLATO trial (n=18 624), reviewers, blinded to study treatment, subclassified direct causes of death and evaluated whether infection or bleeding events contributed to fatal events. RESULTS: Among vascular deaths, there were significantly fewer sudden deaths (63 (0.7%) vs 98 (1.1%), p<0.01) but no significant difference in deaths caused by acute myocardial infarction (179 (1.9%) vs 194 (2.1%), p=0.43) or heart failure (31 (0.3%) vs 42 (0.5%), p=0.20) with ticagrelor compared with clopidogrel. For non-vascular deaths, there was no difference between treatments in deaths directly caused by infection. Although, patients treated with ticagrelor were at lower risk for death where infection was either a direct cause or contributed to death (51 (0.5%) vs 76 (0.8%), HR 0.67 (0.47 to 0.95), p<0.05) but not for bleeding (42 (0.5%) vs 42 (0.5%), HR 0.99 (0.65 to 1.53), p=0.98). CONCLUSIONS: In this post hoc analysis, ticagrelor compared with clopidogrel reduced total and cardiovascular mortality, which appeared to be mainly mediated by a reduction in sudden death. Importantly, bleeding causing or contributing to death did not differ between treatments. CLINICAL TRIAL REGISTRATION NUMBER: NCT00391872 (http://www.clinicaltrial.gov).

Factors contributing to the lower mortality with ticagrelor compared with clopidogrel in patients undergoing coronary artery bypass surgery.

OBJECTIVES: This study investigated the differences in specific causes of post-coronary artery bypass graft surgery (CABG) deaths in the PLATO (Platelet Inhibition and Patient Outcomes) trial. BACKGROUND: In the PLATO trial, patients assigned to ticagrelor compared with clopidogrel and who underwent CABG had significantly lower total and cardiovascular mortality. METHODS: In the 1,261 patients with CABG performed within 7 days after stopping study drug, reviewers blinded to treatment assignment classified causes of death into subcategories of vascular and nonvascular, and specifically identified bleeding or infection events that either caused or subsequently contributed to death. RESULTS: Numerically more vascular deaths occurred in the clopidogrel versus the ticagrelor group related to myocardial infarction (14 vs. 10), heart failure (9 vs. 6), arrhythmia or sudden death (9 vs. 3), and bleeding, including hemorrhagic stroke (7 vs. 2). Clopidogrel was also associated with an excess of nonvascular deaths related to infection (8 vs. 2). Among factors directly causing or contributing to death, bleeding and infections were more common in the clopidogrel group compared with the ticagrelor group (infections: 16 vs. 6, p < 0.05, and bleeding: 27 vs. 9, p < 0.01, for clopidogrel and ticagrelor, respectively). CONCLUSIONS: The mortality reduction with ticagrelor versus clopidogrel following CABG in the PLATO trial was associated with fewer deaths from cardiovascular, bleeding, and infection complications. (Platelet Inhibition and Patient Outcomes [PLATO]; NCT00391872).

Platelet inhibition assessed with VerifyNow, flow cytometry and PlateletMapping in patients undergoing heart surgery.

INTRODUCTION: A substantial number of patients with coronary artery disease undergo cardiac surgery within five days of discontinuing anti-platelet treatment with aspirin and clopidogrel. The aims of this study were to describe the degree of platelet inhibition in patients with dual anti-platelet treatment scheduled for coronary artery bypass graft (CABG) surgery and to investigate whether the measured platelet inhibition correlated to intra- and postoperative risk for bleeding and transfusion requirements. MATERIAL AND METHODS: Sixty patients were included. Platelet inhibition was analysed with flow cytometry including phosphorylation status of the vasodilator-stimulated phosphoprotein (VASP-assay) and two bed-side analyzers, VerifyNow-System and PlateletMapping, a modified thrombelastograph. All 60 patients were analysed with VerifyNow and PlateletMapping, and 48 were analysed with flow cytometry and VASP-assay. RESULTS: There was a correlation between the ADP-receptor inhibition as measured by VASP-assay and VerifyNowP2Y(12) (r = -0.29, p<0.05), and between VASP-assay and the expression of P-selectin (r = 0.29, p<0.05) as measured by flow cytometry when platelets were stimulated with 5 microM ADP. VerifyNowP2Y(12) was the only measurement of platelet inhibition correlated to total blood loss (Spearman r = 0.29, p=0.03) and red blood cell transfusion (Spearman r = 0.43, p<0.01) requirements, although this might be confounded by aprotinin treatment. CONCLUSION: We found a modest agreement between the methods for preoperative platelet inhibition, though not for PlateletMapping-MA(ADP). There was a correlation between preoperative platelet inhibition measured by VerifyNowP2Y(12) and surgical blood loss or transfusion requirements. However, for the individual patient, preoperative use of VerifyNowP2Y(12) as an instrument to decide bleeding and transfusion risk does not seem helpful.