Adding colchicine to aspirin may prevent recurrence of acute pericarditis.
Explore the source record for details and available documents.
Comment↗
Biomedical subjects
Bernhard Maisch
Publications and source records attributed to Bernhard Maisch.
Biventricular stimulation to prevent cardiac desynchronization: rationale, design, and endpoints of the 'Biventricular Pacing for Atrioventricular Block to Prevent Cardiac Desynchronization (BioPace)' study.
Despite the deleterious effects of cardiac dyssynchrony and the positive effects of cardiac resynchronization therapy, patients with high-degree atrioventricular block continue to receive desynchronizing right ventricular (RV) pacing systems. Although it is unclear whether the negative effects of RV pacing and left bundle branch block (LBBB) are comparable, and whether they depend on the presence and the degree of structural heart disease, one may hypothesize that RV pacing may have similar effects to LBBB. In the BioPace trial, the long-term effects of RV pacing vs. biventricular pacing will be prospectively compared in 1200 pacemaker patients with high likelihood of mostly paced ventricular events, regardless of whether in sinus rhythm or in atrial fibrillation (AF). After echocardiographic examination of left ventricular (LV) function, patients will be randomly assigned to the implantation of an RV vs. a biventricular pacing system and followed for up to 5 years. Primary study endpoints are survival, quality of life (QoL), and the distance covered in a 6-min hall walk (6-MHW) at 24 months after implantation. Secondary endpoints are QoL and the 6-MHW result at 12 months after implantation, hospitalization rate, LV dimensions, LV ejection fraction, and the development of chronic AF and other adverse events.
Cardiac Pacing, Artificial↗
Antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with prophylactic cardioverter-defibrillator therapy.
AIMS: Antitachycardia pacing (ATP) has not routinely been used in patients who received implantable cardioverter defibrillators (ICDs) for primary prevention of sudden death. This study investigated the efficacy of empirical ATP to terminate rapid ventricular tachycardia (VT) in heart failure patients with prophylactic ICD therapy. METHODS AND RESULTS: Ninety-three patients with a mean left ventricular ejection fraction of 22 +/- 7% (range: 9-35%) due to nonischemic or ischemic cardiomyopathy received prophylactic ICDs with empiric ATP. At least 2 ATP sequences with 6-pulse burst pacing trains at 81% of VT cycle length (CL) were programmed in one or two VT zones for CL below 335 +/- 23 ms and above 253 +/- 18 ms. Ventricular flutter and fibrillation (VF) with CL below 253 +/- 18 ms were treated in a separate VF zone with ICD shocks without preceding ATP attempts. During 38 +/- 27 months follow-up, 339 spontaneous ventricular tachyarrhythmias occurred in 36 of 93 study patients (39%). A total of 232 VT episodes, mean CL 293 +/- 22 ms, triggered ATP in 25 of 36 patients with ICD interventions (69%). ATP terminated 199 of 232 VT episodes (86%) with a mean CL of 294 +/- 23 ms in 23 of 25 patients (88%) who received ATP therapy. ATP failed to terminate or accelerated 33 of 232 VT episodes (14%) with a mean CL of 287 +/- 19 ms in 12 of 25 patients (48%) who received ATP therapy. CONCLUSIONS: Painfree termination of rapid VT with empirical ATP is common in heart failure patients with prophylactic ICD therapy. The occasional inability of empiric ATP to terminate rapid VT in almost 50% of patients who receive ATP for rapid VT warrants restrictive ICD programming with regard to the number of ATP attempts in order to avoid syncope before VT termination occurs.
Cardiac Pacing, Artificial↗
Activated nuclear transcription factor kappaB in patients with myocarditis and dilated cardiomyopathy--relation to inflammation and cardiac function.
OBJECTIVES AND BACKGROUND: Myocarditis is caused by various agents and autoimmune processes. It is unknown whether viral genome persistence represents inactive remnants of previous infections or whether it is attributed to ongoing adverse processes. The latter also applies to the course of autoimmune myocarditis. One principal candidate for an adverse remodeling is nuclear factor-kappaB (NFkappaB). METHODS: A total of 93 patients with suspected myocarditis/cardiomyopathy was examined. Hemodynamics were assessed by echocardiography as well as right and left heart catheterization. Endomyocardial biopsies were taken from the left ventricle. Biopsies were examined by immunohistochemistry and PCR for viral genomes. Selective immunostaining of activated NFkappaB was performed. RESULTS: NFkappaB was increased in patients with myocarditis when compared with controls (11.1+/-7.1% vs. 5.0+/-5.3%, P<0.005) whereas dilated cardiomyopathy showed no significant increase. Patients with myocarditis and preserved left ventricular function exhibited increased activated NFkappaB when compared with reduced function (r2=0.72, P<0.001). In parallel, inverse correlation of NFkappaB and left ventricular enddiasstolic volume was found (r2=0.43, P<0.02). Increased activated NFkappaB was found in adenovirus persistence when compared with controls (P=0.001). Only a trend of increased NFkappaB activation was seen in cytomegalovirus persistence. Parvovirus B19 persistence did not affect NFkappaB activation. CONCLUSIONS: Increased activation of NFkappaB is related to inflammatory processes in myocarditis. Since activated NFkappaB correlates with left ventricular function, it could be assumed that NFkappaB activation occurs at early stages of inflammation. Potentially, NFkappaB could inhibit loss of cardiomyocytes by apoptosis and protect from cardiac dilation. Since NFkappaB is a crucial key transcription factor of inflammation, its prognostic and future therapeutic relevance should be addressed.
Adult↗
The 103I variant of the melanocortin 4 receptor is associated with low serum triglyceride levels.
CONTEXT: The melanocortin 4 receptor (MC4R) is an essential regulator of energy intake and body weight. Recently, the V103I polymorphism of MC4R has been shown to be negatively associated with body mass index. This suggests that serum lipids and blood pressure in individuals carrying the 103I allele might be influenced as well. OBJECTIVE: The objective of this study was to determine whether the most common polymorphism of the MC4R, V103I, affects serum lipid levels and/or blood pressure. DESIGN, SETTING, AND PARTICIPANTS: The study participants were 1173 consecutive patients undergoing cardiac catheterization; they were genotyped for the rs2229616 G-->A substitution at codon 103 (V103I polymorphism) of the MC4R gene. Patients had strictly fasted for at least 12 h before blood samples were drawn. The average age of the patients was 60.9 yr; 72% were males. MAIN OUTCOME MEASURES: The main outcome measures were body mass index, serum lipids, aortic and systolic blood pressure, and MC4R polymorphism V103I. RESULTS: Heterozygous carriers of the 103I allele had significantly lower triglyceride levels than individuals homozygous for the wild-type allele (127 vs. 168 mg/dl mean total triglyceride; P = 0.001 or 0.009 after Bonferroni adjustment for seven tests). No homozygous carriers of the 103I allele were present in the study population. CONCLUSIONS: Our study suggests an influence of MC4R activity on triglyceride levels in cardiovascular patients.
Blood Pressure↗
TNF-related apoptosis-inducing ligand and its decoy receptor osteoprotegerin in nonischemic dilated cardiomyopathy.
Apoptosis has been attributed an essential role in dilated cardiomyopathy (DCM) recently. We assessed expression of TNF-related apoptosis-inducing ligand (TRAIL) and its decoy receptor osteoprotegerin (OPG) in men with nonischemic DCM, who underwent coronary angiography and endomyocardial biopsy (EMB) after exclusion of coronary artery disease compared to control patients. TRAIL plasma concentrations were elevated in DCM (p=0.02 vs. controls), and were positively correlated with left ventricular enddiastolic diameter (r=0.15, p=0.04), whereas OPG plasma levels did not differ between both groups (p=0.96). In EMB of DCM patients, TRAIL and OPG protein were detected by immunohistochemistry but not in controls. Furthermore, gene expression in EMB or peripheral blood leukocytes (PBL) of DCM patients assessed by real-time PCR showed an increase of TRAIL mRNA in PBL (p=0.01 vs. controls), whereas OPG mRNA was upregulated in endomyocardial specimens (p<0.001 vs. controls). In conclusion, myocardial overexpression of antiapoptotic OPG in DCM patients may represent a compensatory mechanism to limit systemic activation of TRAIL in patients with congestive heart disease.
Adult↗
Matrix metalloproteinases and their inhibitors in malignant and autoreactive pericardial effusion.
Matrix metalloproteinases (MMPs) are proteolytic enzymes essentially involved in tissue remodeling and tumor invasion, and their activity is counterbalanced by endogenous antagonists, the tissue inhibitors of matrix proteinases (TIMPs). Recent reports have suggested a potential role of MMPs in the evolution of pericardial effusion (PE). In this study, we determined the levels of MMP-2 and MMP-9 and their inhibitors TIMP-1 and TIMP-2 in 19 patients who had malignant PE that was confirmed by histology or cytology and 30 patients who had nonmalignant, autoreactive PE compared with pericardial fluid of 19 patients who had preserved left ventricular function and who underwent aortocoronary bypass surgery for control. Samples were assayed by zymography, immunoblotting, and quantitative enzyme-linked immunosorbent assay. We found significantly higher MMP-2 levels in malignant PE than in pericardial fluid (2,906 +/- 348 vs 1,493 +/- 114 ng/ml, p = 0.0005) or autoreactive PE (2,079 +/- 269 ng/ml, p = 0.01). No significant differences in MMP-9 levels were found between malignant PE and autoreactive PE (83 +/- 28.6 vs 106 +/- 30.4 ng/ml, p = 0.22), whereas MMP-9 was below the detection limit in pericardial fluid. No differences in TIMP-1 levels were found across the different study groups, whereas compared with pericardial fluid, TIMP-2 levels were significantly lower in autoreactive PE (113 +/- 18.9 vs 187 +/- 12.2 ng/ml, p = 0.002). In addition, there was a trend to lower TIMP-2 levels in malignant PE (137 +/- 27.1 ng/ml, p = 0.07). The present findings indicate that proteolytic enzymes and their inhibitors are involved in the pathogenesis of PE, with an expression pattern that depends on etiology. The involvement of MMP-2 in the pathogenesis of malignant PE may indicate a potential role of MMP inhibitors in the control of malignant PE.
Biopsy↗
Fatty acid oxidation inhibition with PPARalpha activation (FOXIB/PPARalpha) for normalizing gene expression in heart failure?
Explore the source record for details and available documents.
Animals↗
Prognostic significance of serum cholesterol levels in patients with idiopathic dilated cardiomyopathy.
AIMS: Previous studies indicate that low cholesterol levels are associated with adverse prognosis in heart failure patients, because elevated lipoprotein levels may negate bacterial endotoxin load induced by gastrointestinal congestion. METHODS AND RESULTS: We examined the prognostic significance of lipid levels in a cohort of 422 patients with idiopathic dilated cardiomyopathy (iDCM) [50+/-12 years, 342 males, 80 females, left ventricular ejection fraction (LV-EF): 31.6+/-10.6%]. During 42 months of follow-up, 86 patients (20.3%) died or received a heart transplant. In univariate Cox regression analysis, reduced LV-EF, high New York Heart Association (NYHA) class, and increased LV end-diastolic diameter (LVEDD) were strong risk factors associated with that endpoint, whereas decreased total cholesterol, HDL-cholesterol, and apoprotein I levels were identified as weak risk predictors. After step-wise multivariable analysis, only LVEDD, NYHA class, and LV-EF emerged as parameters independently contributing to the model predicting risk for death or heart transplantation (P<0.05). Cholesterol levels were positively associated with LV-EF and negatively associated with LVEDD (P<0.05). Circulating sCD14 levels, a marker of endotoxin exposure, were related to cholesterol levels (P<0.05) and LV-EF (P<0.05). CONCLUSION: Decreased cholesterol levels do not independently predict adverse prognosis in patients with iDCM. Our findings indicate that low cholesterol levels are dependent on the severity of cardiac disease.
Adult↗
Recurrent pericarditis: mysterious or not so mysterious?
Explore the source record for details and available documents.
Adrenal Cortex Hormones↗
Right ventricular cardiac myxoma. Diagnostic usefulness of cardiac magnetic resonance imaging.
BACKGROUND: Cardiac myxomas are the most common type of cardiac tumors. About 75-85% of cardiac myxomas originate in the left atrium, 15-20% in the right atrium. Most myxomas arise from the interatrial septum adjacent to the fossa ovalis. Only 3-4% are found in the left and right ventricle each. Although myxomas are histologically benign, they may be fatal because of their strategic position. CASE STUDY: The authors report on a 24-year-old patient with stabbing thoracic pain and dyspnea due to pulmonary thromboembolism that was caused by an atypically localized myxoma at the right ventricular apex originating from the interventricular septum. The diagnosis was based on cardiac magnetic resonance (CMR) imaging. Superior to echocardiography, CMR could strengthen the diagnostic accuracy by additional information on tissue characterization using different imaging sequences. Typically for cardiac myxomas, contrast enhancement was moderate and delayed enhancement was found in the outer circumferential tumor margins only. CONCLUSION: High spatial resolution and multiplane imaging combined with different acquisition patterns of CMR achieve a global view of the heart that seems to be useful for diagnosing cardiac tumorous masses.
Adult↗
Management of pericardial effusion the role of echocardiography in establishing the indications and the selection of the approach for drainage.
Explore the source record for details and available documents.
Drainage↗
[A paradigm change in German academic medicine. Merger and privatization as exemplified with the university hospitals in Marburg and Giessen].
1. The intended fusion of the university hospitals Marburg and Giessen in the state of Hessia is "a marriage under pressure with uncalculated risk" (Spiegel 2005). In the present political and financial situation it hardly appears to be avoidable. From the point of the view of the faculty of medicine in Marburg it is difficult to understand, that the profits of this well guided university hospital with a positive yearly budget should go to the neighboring university hospital which still had a fair amount of deficit spending in the last years.2. Both medical faculties suffer from a very low budget from the state of Hessia for research and teaching. Giessen much more than Marburg, have a substantial need for investments in buildings and infrastructure. Both institutions have a similar need for investments in costly medical apparatuses. This is a problem, which many university hospitals face nowadays.3. The intended privatisation of one or both university hospitals will need sound answers to several fundamental questions and problems:a) A privatisation potentially endangers the freedom of research and teaching garanteed by the German constitution. A private company will undoubtedly influence by active or missing additional support the direction of research in the respective academic institution. An example is the priorisation of clinical in contrast to basic research.b) With the privatisation practical absurdities in the separation of research and teaching on one side and hospital care on the other will become obvious with respect to the status of the academic employees, the obligatory taxation (16%) when a transfer of labor from one institution to the other is taken into account. The use of rooms for seminars, lectures and bedside with a double function for both teaching, research and hospital care has to be clarified with a convincing solution in everyday practice.c) The potential additional acquisition of patients, which has been advocated by the Hessian state government, may be unrealistic, when the 4th biggest university hospital in Germany will be created by the merger. University hospitals recrute the patients for high end medicine beyond their region because of the specialized academic competence and advanced technical possibilities. Additional recruitment of patients for routine hospital can hardly be expected.d) A private management will have to consider primarily the "shareholder value", even when investing in infrastructure and buildings, as it can be expected for one partner. On the longterm this will not be possible without a substantial reduction of employees in both institutions. There are, however, also substantial efforts of some private hospital chains in clinical research, e. g. by Helios in Berlin and Rhön Gmbh at the Leipzig Heart Center.e) There is a yet underestimated but very substantial risk because of the taxation for the private owner when academic staff is transferred from the university to hospital care in their dual function as academic teachers and doctors. This risk also applies for the university if the transfer should come from hospital to the university. These costs would add to the financial burden, which has to be carried in addition to the DRGs.
Academic Medical Centers↗
Lipids and lipoproteins in women.
Atherosclerosis and coronary artery disease (CAD) are the main causes of death in the Western world, for both men and women. However, in premenopausal women CAD is less frequent than in men, but in elderly women (e.g., > 75 years) myocardial infarction (MI) occurs even more often than in men. In summary, women suffer from CAD and MI but at a later age than men. Therefore it is important to observe and compare the cardiovascular risk factors in women and men. The typical CAD risk factors such as hyperlipidemia, smoking, arterial hypertension, diabetes mellitus, obesity, physical inactivity, and unhealthy nutrition are increasingly important for both genders. Many of these factors are comparable between men and women, but due to hormonal influences especially the lipoprotein metabolism shows some striking differences between men and women, but interestingly enough also between pre- and postmenopausal women. Therefore this paper will focus especially on the gender-specific differences in lipid metabolism as a potential target which might explain both the gender-specific and also pre- and postmenopausal differences in the occurrence of CAD.
Coronary Artery Disease↗
[Women and pericardial neoplastic manifestations of the heart and pericardium].
BACKGROUND: In every year since 1984, cardiovascular disease has claimed the lives of more females than males. In the Western world more than 450,000 women succumb to heart disease annually. Despite the proportions, most women believe that heart disease is a man's disease and that they will die of breast cancer. Data on epidemiology and incidence are rare: there is only an estimated incidence of cardiac neoplasm at necropsy ranging from 0,001% to 0,3%. The majority of the primary tumors are benign. Females are affected more often than males. The most common tumor entity is benign cardiac myxoma. Malignant heart tumors are less common. Most often they are different types of sarcomas, which have a poor outcome and affect more males than females. Metastatic tumors of the heart are 100 times more common than the primary ones. They originate mainly from melanomas, leukemias, lymphomas, and cancer, especially of the lung or breast. Indeed in women breast cancer is the most common metastatic tumor associated with pericardial effusion. To prevent death from tamponade, pericardiocentesis, in addition to the systemic chemotherapy, is mandatory, best when instillation of chemotherapeutics (cisplatin or thiotepa) or radioisotopes is given into the pericardial sac to prevent recurrence of the effusion. However, more of the malignant tumors may be curable if exactly diagnosed at an earlier stage. METHODS: A retrospective study was conducted of all patients with cardiac and pericardial neoplasm exactly diagnosed by endomyocardial or epicardial biopsy and pericardiocentesis, using hospital medical records and a biopsy and pericardiocentesis registry from 2000-2005 with 297 patients. Pericardial effusion and biopsy analyses included biochemistry, cytology, serology, microbiology, histology, immunohistology, and polymerase chain reaction (PCR). All patients were investigated in relation to Herzmetasgender differences to histopathologic findings, clinical presentation and outcome. RESULTS: In 76 cases (25.6%) a neoplasm was the reason for a pericardial effusion. 36 women suffered from the breast carcinoma (47%) and 40 males lung cancer (42%) as the firstly metastatic tumor. There was no recurrence of a relevant pericardial effusion in patients who were treated by intrapericardial instillation of cisplatin (30 mg/m2 body surface in 100 ml 0.9% NaCl). CONCLUSION: Females are more often affected by primary cardiac tumors than males with an excellent outcome. By contrast, the preventive checkup and aftercare will gain more prognostic importance, especially in case of breast cancer, to earlier recognize a secondary cardiac neoplasm by biopsy and pericardiocentesis with intrapericardial treatment of neoplastic pericarditis.
Breast Neoplasms↗
[Women and autoimmune diseases with cardiovascular manifestations].
Women's greater susceptibility to autoimmune diseases has been recognized for more than 100 years. And although the basic immune response (including a more vigorous immune response and increased antibody production) has been known to differ between men and women, conclusive pathophysiological explanations for this phenomenon are still lacking. Experimental work done in animal models have revealed a profound influence of sex hormones on the susceptibility to autoimmune diseases and on clinical disease via direct and indirect signaling pathways. Apart from sex hormones additional factors seem to participate in the pathogenesis of autoimmune diseases, which remain to be elucidated ("so far, you cannot explain autoimmunity [only] with estrogen" [lockshin]).
Animals↗
Inflammatory dilated cardiomyopathy (DCMI).
Cardiomyopathies are heart muscle diseases, which have been defined by their central hemodynamics and macropathology and divided in five major forms: dilated (DCM), hypertrophic (HCM), restrictive (RCM), right ventricular (RVCM), and nonclassifiable cardiomyopathies (NCCM). Furthermore, the most recent WHO/WHF definition also comprises, among the specific cardiomyopathies, inflammatory cardiomyopathy as a distinct entity, defined as myocarditis in association with cardiac dysfunction. Idiopathic, autoimmune, and infectious forms of inflammatory cardiomyopathy were recognized. Viral cardiomyopathy has been defined as viral persistence in a dilated heart. It may be accompanied by myocardial inflammation and then termed inflammatory viral cardiomyopathy (or viral myocarditis with cardiomegaly). If no inflammation is observed in the biopsy of a dilated heart (< 14 lymphocytes and macrophages/mm(2)), the term viral cardiomyopathy or viral persistence in DCM should be applied according to the WHF Task Force recommendations. Within the German heart failure net it is the authors' working hypothesis, that DCM shares genetic risk factors with other diseases of presumed autoimmune etiology and, therefore, the same multiple genes in combination with environmental factors lead to numerous different autoimmune diseases including DCM. Therefore, the authors' primary goal is to acquire epidemiologic data of patients with DCM regarding an infectious and inflammatory etiology of the disease. Circumstantial evidence points to a major role of viral myocarditis in the etiology of DCM. The common presence of viral genetic material in the myocardium of patients with DCM provides the most compelling evidence, but proof of causality is still lacking. In addition, autoimmune reactions have been described in many studies, indicating them as an important etiologic factor. Nevertheless, data on the proportion of patients, in whom both mechanisms play a role are still missing.A pivotal role for autoimmunity in a substantial proportion of patients with DCM is supported by the presence of organ-specific autoantibodies, inflammatory infiltrates and pro-inflammatory cytotoxic cytokines. Furthermore, familial occurrence of DCM has been described in about 20-30% of cases, with the presence of autoantibodies and abnormal cytokine profiles in first-degree relatives with asymptomatic left ventricular enlargement. This suggests the involvement of a disrupted humoral and cellular immunity early in the development of the disease. A similar pattern of humoral and cellular immune dysregulation has been described in other autoimmune diseases. There is considerable evidence that genetic factors play an important role in the pathogenesis of DCM, either as contributors to the susceptibility to environmental factors or as determinants of functional and structural changes that characterize the phenotypic expression of the disease.Yet, it is not known whether the susceptibility to immunologically mediated myocardial damage reflects the presence of genetic risk factors shared by other autoimmune diseases. Preliminary investigations suggest, that this is the case, because the frequency of autoimmune disorders other than DCM was higher in first-degree relatives of the subjects with DCM including juvenile diabetes, rheumatoid arthritis, thyroiditis, psoriasis, and asthma. The nature of the genetic risk is undetermined and probably involves genes in the major histocompatibility (MHC) locus as well as other susceptibility loci. Therefore, the authors started their investigation with the search for MHC class 2 DQ polymorphisms in the peripheral blood of patients with DCM in parallel to the search for new interesting susceptibility loci by the use of the microarray analysis regarding genes responsible for inflammatory and autoimmune diseases. By this approach a new insight in the familial clustering of other autoimmune diseases in patients with DCM and in genetic predisposition can be expected.
Cardiomyopathy, Dilated↗
Indications for angiography subsequent to coronary artery bypass grafting.
BACKGROUND: Postoperative myocardial infarction is a rare, but potentially severe complication after coronary artery bypass grafting (CABG). Early markers for coronary bypass graft failure or native vessel occlusion are required, because immediate intervention could prevent major myocardial damage. METHODS: One thousand patients with coronary artery disease consecutively underwent CABG. Postoperative coronary angiography was performed in 40 patients with suspected myocardial ischemia. Creatine kinase (CK), CK-MB, leukocyte count, C-reactive protein (CRP), lactate dehydrogenase (LDH), and glutamate-oxalacetate transaminase (GOT) were assessed at 0, 6, 12, 24, 48, and 72 hours after CABG as well as 12-lead standard electrocardiography (ECG). RESULTS: Postoperative angiography of 40 patients with suspected myocardial infarction revealed graft failure or occluded native vessels in 13 (32.5%) individuals. Patients with graft or vessel occlusion presented elevated (P < .005) leukocyte counts (17,215 +/- 6632 vs 10,773 +/- 3902 G/L) immediately after CABG. CK-MB concentrations differed ( P < .05) at 6 hours after CABG (54 +/- 48 vs 30 +/- 18 U/L). CK, CRP, LDH, and GOT did not show any differences between both groups. Frequency of ECG ST-segment elevation was increased (P < .05) in ischemic patients (69.2% vs 29.6%). CONCLUSIONS: Common signs of myocardial ischemia usually allow to diagnose unstable angina or myocardial infarction under native conditions. In contrast, these criteria frequently fail after CABG. Combined diagnostic criteria of elevated leukocytes (>14,000 G/L, at hour 0) and either ST elevation or CK-MB concentrations >35 U/L (at hour 6) at least seem to be very useful in detecting myocardial infarction after bypass grafting. In parallel, CK-MB elevation (>70 U/L, at hour 6) alone seems to predict ischemia. Both criteria should indicate angiography and potential revascularization. If these conditions were not fulfilled, the risk of perioperative myocardial infarction appears to be moderate.
Aged↗