Post PCI atrial fibrillation

Atrial fibrillation (AF) is a major arrhythmia with a high prevalence among population. AF is not uncommon in the setting of coronary artery disease, including myocardial infarction (MI) and acute coronary syndromes (ACS). Percutaneous coronary interventions (PCI) have significantly improved outcomes of patients with acute MI and acute coronary syndromes. Nevertheless, the AF was reported to occur in patients with MI and ACS undergoing PCI. New onset AF after PCI for MI and ACS, though being infrequent, was associated with worse clinical course and prognosis. The predictive value of AF has tendency to change in parallel with improvements of reperfusion strategies and comprehensive treatment. Observational studies suggest better patency of culprit vessels achieved by PCI was accompanied by improvement in signal-averaged electrocardiography indices of atrial electrophysiological properties and higher rate of restoration of sinus rhythm during primary PCI as compared with thrombolysis. The adequate management of arrhythmia is required to reduce the risk of complications.     

Potential precipitating factors of the onset of myocardial infarction.

Myocardial infarction (MI) usually results from thrombotic coronary artery occlusion at the site of a ruptured atherosclerotic plaque. The factors responsible for triggering MI are not known but conditions that increase serum catecholamines may be involved. Accordingly, the authors prospectively evaluated the presence of factors that may increase catecholamines immediately prior to MI in 186 patients. Myocardial infarction was documented by a rise in serum CK-MB. There were 149 men and 37 women, aged 57 +/- 12 (mean +/- SD) years. All patients were interviewed within 72 hours of admission concerning strenuous physical activity, emotional stress, and assumption of the upright posture immediately prior to the onset of symptoms. Seventy-five (40%) patients had one or more of these factors immediately prior to the onset of MI chest pain. Fourteen (8%) experienced acute emotional upset; 28 (15%) were involved in strenuous physical activity; and 39 (21%) had suddenly changed position. In the latter group, 18 changed from being supine for more than 1 hour to standing; three rose from supine to sitting; and 18 changed from prolonged sitting (greater than 60 minutes) to standing. The conclusion is that a potential triggering factor is present in many patients immediately prior to the onset of MI. A sudden change in position is the most frequent potential trigger, typically occurring the morning after awakening from sleep.     

Severe spontaneous three-vessel coronary artery spasm

Coronary artery spasm is usually defined as a focal constriction of a coronary artery segment, reversible, and causing myocardial ischaemia by coronary blood flow restriction. Sometimes this condition is not focal and can compromise all the coronary tree. This is a very rarely described event. Generally, coronary vasospasm may occur spontaneously or induced, either physically by catheter, physiological manoeuvres (hyperventilation), or by pharmacological agents. It may also occur with or without underlying atheromatous coronary disease. The mechanism of coronary spasm remains unclear but endothelial dysfunction seems to be the main triggering factor in all causes.     

Autonomic neurocardiogenic syndrome is stonewalled by the universal definition of myocardial infarction

Myocardial infarction(MI) is defined as myocardial cell death due to prolonged myocardial ischemia. Clinically, troponin rise and/or fall have become the"defining feature of MI" according to the universal definition of MI(UD-MI).Takotsubo syndrome(TS) and TS-related disease conditions also cause troponin elevation with typical rise and/or fall pattern but through a mechanism other than coronary ischemia. By strict application of the clinical diagnostic criteria for type-1 MI, type-2 MI, type-3 MI, and MI with non-obstructive coronary arteries according to the UD-MI including the fourth one published recently, TS and most of the 26 other causes of troponin elevation mentioned in the fourth UD-MI may erroneously be classified as MI. The existing evidence argues for the case that TS by itself is not a MI. Hyper-activation of the autonomic-sympathetic nervous system including local cardiac sympathetic hyper-activation and disruption with nor-epinephrine churn and spillover is the most probable cause of TS. This autonomic neuro-cardiogenic(ANCA) mechanism results in myocardial "cramp"(stunning), the severity and duration of which depend on the degree of the sympathetic-hyperactivation and nor-epinephrine spillover. The myocardial cramp may squeeze the cytosolic free troponin pools causing mild to moderate troponin elevation in TS and TS-related disease conditions. This ANCA syndrome, which has hitherto been enveloped by the UD-MI over more than one decade, may occur in acute, recurrent, and chronic forms. In this critical review,the controversies of UD-MI, evidence for ANCA syndrome, and a hypothetical mechanism for the troponin elevation in ANCA syndrome are provided.     

Effects of the Mueller maneuver on global and regional left ventricular function in angina pectoris with or without previous myocardial infarction

In patients with coronary artery disease, left ventricular (LV) regional wall akinesia can develop during the Mueller maneuver. The present study determines if the presence of myocardial ischemic disease with no infarction is a sufficient condition for this to occur, or if the presence of prior acute myocardial infarction (MI) is necessary. In men, first-pass radionuclide ventriculography was performed in the 30 degree left anterior oblique supine position to measure LV ejection fraction, end-diastolic and end-systolic volumes and heart rate, and to obtain an image of the LV cavitary perimeter. This procedure was performed in 4 subject groups: 13 normal volunteers, 25 patients with coronary artery disease but no prior MI, 13 patients with coronary artery disease and prior nontransmural MI, and 36 patients with coronary artery disease and prior transmural MI. All patients had angina and underwent routine contrast coronary angiography; 60 also underwent contrast coronary angiography; 60 also underwent contrast LV angiography. Ejection fraction decreased during the Mueller maneuver in each of all the coronary artery disease groups (p less than 0.01), but not in the normal subjects. Heart rate increased in groups 1, 2 and 4 (p less than 0.01), and end-diastolic volume decreased in all 4 groups (p less than 0.01), whereas end-systolic volume did not change. Only in group 4 did regional wall akinesia develop (17 patients) during the Mueller maneuver. Among patients who had akinesia during the Mueller maneuver and also underwent routine contrast ventriculography, half of the akinetic segments were not seen on routine contrast study, but were seen only on radionuclide ventriculography during the Mueller maneuver.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of p38alpha MAPK in cardiac apoptosis and remodeling after myocardial infarction

Acute coronary occlusion results in ischemia-mediated death of cardiomyocytes. In the days and weeks following myocardial infarction (MI), left ventricular remodeling occurs that is characterized by persistent cardiomyocyte apoptosis, thinning and fibrosis at the site of infarction, ventricular chamber dilatation, and growth of remaining viable cardiomyocytes. The p38 mitogen-activated protein kinase (MAPK) signaling cascade has been implicated in the remodeling process. In this work, mice with cardiac-specific expression of a dominant negative mutant form of p38 MAPK (DN-p38alpha) were subjected to MI by occlusion of the left coronary artery. Acute ischemia area was determined by transthoracic echocardiography 2 h after MI surgery, and was found to be nearly identical in DN-p38 mice and their wild-type littermates. Seven days after MI, mice were subjected to repeat echocardiography and histological examination of infarct size. DN-p38 mice had markedly reduced infarct size and increased ventricular systolic function 7 days after MI when compared to wild-type littermates. In addition, DN-p38 mice had less cardiomyocyte apoptosis than wild-type mice in the infarct border zone. Recently, it was discovered that Bcl-X(L) deamidation occurs in vivo, and this results in Bcl-X(L) degradation that sensitizes cells to apoptosis by enhancing BAX activity. Bcl-X(L) deamidation was found to occur in the cardiac tissue of wild-type mice after MI, but was reduced in DN-p38 mice. These results establish that p38 MAPK activity is required for pathological remodeling after MI and suggest that p38 MAPK may promote cardiomyocyte apoptosis through Bcl-X(L) deamidation.     

The paraoxonase Leu-Met54 and Gln-Arg191 gene polymorphisms are not associated with the risk of coronary heart disease

BACKGROUND: Evidence has been presented that gene polymorphisms (PON54 L/M, PON191 Q/R) of paraoxonase are risk factors of coronary heart disease. RESULTS: We determined both PON genotypes in 535 male individuals who were free of vascular disease and in 2249 male subjects who underwent coronary angiography, and analysed the relation of both gene variations to CAD and MI. Both gene polymorphisms were in linkage disequilibrium (P<0.0001). Coronary artery disease: the PON54 gene polymorphism was not associated with an increased risk of CAD. In the total sample and also in younger subjects, an association of the PON191 gene variation with the risk of CAD was not detected when the control group of individuals without coronary heart disease was compared with patients with at least one diseased vessel (verified by coronary angiography). In individuals younger than 62 years, a moderate increase in the relative risk of CAD associated with the PON191 R allele (1.45 (1. 08-1.95); P=0.015) were found, when subjects without vessel disease (verified by coronary angiography) were compared with CAD patients. Myocardial infarction: an association of the PON54 gene variation with MI was not detected when the control group of individuals without coronary heart disease were compared with patients with at least one MI. A marginal increase in the risk of MI associated with the PON54 LL genotype (OR 1.27 (1.05-1.51); P=0.011) were detected when patients without MI but with coronary angiography were compared with MI positive patients. Subgroup analyses of low- and high-risk populations did not reveal any association of both PON gene polymorphisms with CAD or MI. CONCLUSION: The present findings do not strengthen the hypothesis that the paraoxonase gene polymorphisms are independently associated with coronary heart disease indicating that these gene variations are of little usefulness as genetic markers of cardiovascular disease.     

"Broken heart syndrome": catecholamine surge or aborted myocardial infarction?

Takotsubo cardiomyopathy, also called transient left ventricular apical ballooning or "broken heart syndrome", is a cardiac condition that mimics the clinical presentation of acute coronary syndrome but without any evidence of obstructive atherosclerotic coronary artery disease. An episode of intense emotional or physiologic stress, serving as the nidus for a catecholamine surge, has been reported prior to presentation and is presumed to be the triggering factor playing the pathogenic role. We report a unique case of Takotsubo cardiomyopathy without any known precipitating factors. After reviewing multiple case reports and review articles, the evidence supporting a "catecholamine surge" is empirically plausible; however, our case calls this theory into question. The "aborted MI" hypothesis is more convincing as an all-inclusive nidus for the pathogenesis and clinical presentation described in Takotsubo syndrome. More detailed studies and research are needed to ascertain the pathogenesis and optimal management of this syndrome.     

Myocardial infarction during giant cell arteritis: A cohort study

BackgroundCardiovascular risk is increased in giant cell arteritis (GCA). We aimed to characterize myocardial infarction (MI) in a GCA cohort, and to compare the GCA and non-GCA population affected by MI.MethodsIn patients with a biopsy-proven diagnosis of GCA between 1 January 2001 and 31 December 2016 in Côte D'Or (France), we identified patients with MI by crossing data from the territorial myocardial infarction registry (Observatoire des Infarctus de Côte d'Or) database. Five controls (non-GCA + MI) were paired with one case (GCA + MI) after matching for age, sex, cardiovascular risk factors and prior cardiovascular disease. MI were characterized as type 1 MI (T1MI), resulting from thrombus formation due to atherothrombotic disease, or type 2 MI (T2MI), due to a myocardial supply/demand mismatch. GCA-related MI was defined as MI occurring within 3 months of a GCA flare (before or after).ResultsAmong 251 biopsy-proven GCA patients, 13 MI cases were identified and paired with 65 controls. MI was GCA-related in 6/13 cases, accounting for 2.4% (6/251) of our cohort. T2MI was more frequently GCA-related than GCA-unrelated (80% vs. 16.7%, p = 0.080), and GCA diagnosis was the only identified triggering factor in 75% of GCA-related T2MI. GCA-unrelated MI were more frequently T1MI and occurred in patients who had received a higher cumulative dose of prednisone (p = 0.032). GCA was not associated with poorer one-year survival.ConclusionsGCA-related MI are mainly T2MI probably caused by systemic inflammation rather than coronaritis. GCA-unrelated MI are predominantly T1MI associated with atherothrombotic coronary artery disease.     

血管紧张素转换酶基因I/D多态性及其血清活性与冠心病的关系

目的 :从分子遗传水平探讨血管紧张素转换酶与冠心病的关系及其对冠状动脉病变程度的预测价值。方法 :3 45例患者包括对照患者 95例、心绞痛患者 10 0例及陈旧性心肌梗死患者 15 0例 ,通过两次聚合酶链反应确定血管紧张素转换酶基因型 ,并测定血清血管紧张素转换酶水平。为分析血管紧张素转换酶基因型与冠心病、心肌梗死的相关性 ,将心绞痛患者与陈旧性心肌梗死患者合称冠心病患者 ,对照患者与心绞痛患者合称非心肌梗死患者。结果 :血管紧张素转换酶活性在对照患者、心绞痛患者及心肌梗死患者间无统计学差异。血管紧张素转换酶基因DD、DI和II型的血清血管紧张素转换酶活性有显著性差异 ,经SpearmanRankCorrelation分析 ,血管紧张素转换酶活性与D等位基因数目存在等级相关 ,相关系数 0 2 2 5 ,P <0 0 0 1。血管紧张素转换酶基因型分布在对照患者与冠心病患者、心肌梗死患者与非心肌梗死患者间无显著性差异 ,然而经Logistic回归分析发现 ,在排除其他因素影响下血管紧张素转换酶基因DD型与II型相比 ,对冠心病及心肌梗死的危险性明显增加 ,调整后的OR值分别为 2 2 9及 1 68(P <0 0 5 ) ,提示血管紧张素转换酶基因DD型是冠心病、心肌梗死发生的危险因素。血管紧张素转换酶基因型分布及血清水平均与冠状动     

Myocardial infarction with normal coronary angiography compared with severe coronary artery disease without myocardial infarction: the crucial role of smoking

BACKGROUND: Why do some patients suffer acute myocardial infarction (MI) despite angiographically normal coronary arteries (NL + MI) whereas others enjoy an acute MI-free life despite extensive three-vessel disease (3VD-MI)? The present study contrasts these two groups to identify some differences in the risk profile. METHODS: In 10,000 patients admitted to the cardiology service, a first MI was confirmed in 2356 patients, of whom 1609 underwent coronary angiography. In 77 patients with MI, coronary angiography was found to be entirely normal (NL + MI, 77/1609, 4.1%). These were contrasted to 123 patients with severe three-vessel coronary disease but no MI (3VD-MI). RESULTS: Patients with NL + MI were 13 years younger (42 +/- 8.3 vs 55 +/- 10.5, P < 0.05), with 33 patients (43%) under the age 40 years, in contrast to only 9 patients (7.3%) in the 3VD group being this age. Patients with NC + MI were more often current smokers (80.5% vs 29% in the 3VD group; P < 0.01). Patients with 3VD-MI were, on the other hand, more often diabetic (54% vs 9% in the NL + MI group; P < 0.01) and had a higher cholesterol level (5.6 +/- 1.1 vs 4.9 +/- 1.0 Mmol/l, P < 0.01) as well as a higher incidence of chronic stable angina (52% vs 22%; P < 0.01) and heart failure (6% compared with 0% in the NL + MI group). Sixty-one out of 77 (79%) NL + MI patients had a single risk factor, and in 87%, this was smoking alone. Diabetes mellitus was rare and never occurred alone in this group. CONCLUSION: In patients who suffer MI despite normal coronary angiography, smoking is a major risk factor: In contrast, in patients with extensive coronary artery disease on angiography but no MI, diabetes rather than smoking is the dominant risk factor. The findings of this study support the view that the risk factors for stable and unstable coronary artery disease are different, as reflected by the contrast of the above groups at the extremes of the spectrum. Smoking appears to be a major risk factor for acute MI (even with normal coronary angiography), whereas diabetes is a major risk factor for more severe but more stable coronary artery disease.     

Circadian variation and triggering of cardiovascular events.

Myocardial infarction and sudden cardiac death demonstrate a marked circadian variation with an increased risk during the morning after awakening and arising. The recognition of the morning increase of acute cardiovascular events has convinced many that they may be triggered by morning activities. It is of note, however, that cardiovascular events occur throughout the day--even if at lower frequency compared with the morning. There is a strong association between external triggers and the onset of myocardial infarction and sudden cardiac death beyond what is to be expected by chance alone. The magnitude of this association (relative risk two- to threefold) is comparable with the known long-term risk factors of cardiac disease. Trigger factors occur relatively frequently and may play a causative role in up to 20% of cases of acute coronary syndromes. Physical exertion, bursts of anger and sexual activity have been proved to have triggering potential. Other possible triggers include external and environmental events such as earthquakes, war threat and climatic factors. The pathophysiological links between external triggers and the onset of cardiovascular events are important in addressing the question of a causal relationship between triggers and disease onset and in perhaps improving preventive strategies.     

Comparison of exercise electrocardiography and quantitative thallium imaging for one-vessel coronary artery disease

The relative value of exercise electrocardiography and computer analyzed thallium-201 imaging was compared in 124 patients with 1-vessel coronary artery disease (CAD). Of these, 78 had left anterior descending (LAD), 32 right and 14 left circumflex (LC) CAD. In patients with no previous myocardial infarction (MI), thallium imaging was more sensitive than the electrocardiogram (78% vs 64%, p less than 0.01), but in patients with previous MI, sensitivity was similar. Further, thallium imaging was more sensitive only in LAD and LC disease. Redistribution was compared with ST-segment depression as a marker of ischemia. Only in patients with prior MI (76% vs 44%, p less than 0.01) and only in LC and right CAD did redistribution occur more often than ST depression. Thallium imaging was more accurate in localizing stenoses than the electrocardiogram (p less than 0.001), but did not always correctly predict coronary anatomy. Septal thallium defects were associated with LAD disease in 84%, inferior defects with right CAD in 40% and posterolateral lesion defects with LC CAD in 22%. The results indicate the overall superiority of thallium imaging in 1-vessel CAD compared with exercise electrocardiography; however, there is a wide spectrum of extent and location of perfusion defects associated with each coronary artery. Thallium imaging complements coronary angiography by demonstrating the functional impact of CAD on myocardial perfusion.     

Heart failure as an endpoint in heart failure and non-heart failure cardiovascular clinical trials: the need for a consensus definition.

Specific criteria have been established to define the occurrence of myocardial infarction (MI) and stroke in cardiovascular clinical trials, but there is not a consistent definition for heart failure. Heart failure events appear to occur at a rate that is similar to stroke and MI in trials of hypertension, hyperlipidaemia, diabetes, and coronary heart disease, yet a consistent approach to defining heart failure events has not yet been realized. The wide range of definitions used in clinical trials makes it difficult to interpret new data in the context of existing literature. This inconsistency has led to challenges in determining the incidence of heart failure in cardiovascular studies and the effects of interventions on these endpoints. This paper examines issues related to defining heart failure events in cardiovascular clinical trials and presents a definition to formally address this issue.     

风湿性心脏病合并非冠状动脉粥样硬化性心肌梗死的临床及冠脉造影分析

目的探讨慢性风湿性心脏病（风心病）合并心肌梗死的原因、临床特征、冠状动脉造影表现及治疗.方法回顾性分析18例风心病合并心肌梗死患者的临床和冠脉造影资料.结果18例患者中二尖瓣病变15例（83.3%）,其中5例合并主动脉瓣病变;单纯主动脉瓣病变3例;11（61.1%）例已行瓣膜置换术,服用华法令治疗,国际标准比值（INR）维持在2.0～2.5.合并心房颤动15例（83.3%）.18例患者均有突发胸痛病史,心电图显示前壁心肌梗死13例（72.2%）,下壁心肌梗死5例（27.8%）,其中Q波心梗7例（38.9%）,非Q波心梗11例（61.1%）.伴有心肌酶增高.冠状动脉造影显示冠脉正常14例（77.8%）,4例为急性栓塞,其中1例发生于常规冠脉造影中,另3例胸痛时造影分别为对角支、前降支及右冠脉堵塞,经介入治疗再通.全部患者存活.结论并发于风心病的心肌梗死很少见,冠状动脉栓塞是引起心肌梗死的原因,梗死部位多为前壁,延迟冠脉造影多数正常.     

Predictors of angina pectoris versus myocardial infarction from the Women's Health Initiative Observational Study

Although risk factors for acute coronary syndromes have been extensively studied, characteristics distinguishing women who will develop unstable angina rather than acute myocardial infarction (MI) are less well understood. This analysis evaluates baseline demographic, physical, and medical characteristics as predictors of angina versus MI in the Women's Health Initiative Observational Study. During a prospective 4.5-year follow-up of 92,152 postmenopausal women, 1,527 hospitalizations for angina and 797 for MI were confirmed by centrally trained physician adjudicators. In a multivariate analysis of women with incident angina or MI, high cholesterol (odds ratio [OR] 0.62, 95% confidence interval [CI] 0.47 to 0.80; p = 0.0004) and prior coronary disease (OR 0.70, 95% CI 0.55 to 0.89; p = 0.004) independently predicted angina (referent), whereas current cigarette smoking (OR 1.60, 95% CI 1.13 to 2.26; p = 0.007) and diabetes mellitus (1.44, 95% CI 1.10 to 1.87; p = 0.007) predicted MI. Older age and hypertension were independently, but less strongly, predictive of MI. Aspirin or statin use, physical activity, body mass index, and educational levels were not independently associated with one or the other type of acute coronary syndrome. Thus, specific risk factors strongly and independently predicted whether women with an acute coronary syndrome would present with angina or with MI.     

Acute myocardial infarction in hemoglobin SC disease

Although there are reports of myocardial infarction (MI) in patients with sickle cell diseases, an antemortem diagnosis of acute MI in a patient with compound heterozygous hemoglobin SC disease has not been reported. Herein, we present a patient with hemoglobin SC who suffered an acute MI. She had typical chest pain for myocardial ischemia, associated with ST elevations on the electrocardiogram (EKG) and elevations of cardiac injury markers diagnostic of infarction. The patient was treated with conventional therapies for acute coronary syndrome and also emergent red blood cell exchange. Interestingly, coronary angiography was completely normal in this patient. Potential mechanisms and management for acute MI in patients with sickle cell disease are discussed.     

In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF).

The relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.     

Genetics of platelet glycoprotein receptors: risk of thrombotic events and pharmacogenetic implications.

Platelet aggregation and coronary thrombosis have a central role in the development of acute coronary syndromes and myocardial infarction (MI). Therapies aimed at inhibiting platelet aggregation have shown great benefit in individuals with coronary disease or with multiple risk factors for coronary disease. Genetic variation in platelet surface receptors mediating thrombus formation has been suggested to be associated with platelet hyperreactivity, with increased risk of MI and possibly with the benefit received from various antithrombotic drug treatments. This review focuses on discrepancies and their likely explanations in studies on platelet glycoprotein genetics. Current knowledge on important issues concerning coronary event phenotypes and pharmacogenetics is analyzed. Possible future applicability of these data to patient treatment is also discussed.     

Diagnostic and Therapeutic Implications of Type 2 Myocardial Infarction: Review and Commentary

The Task Force for the Universal Definition of Myocardial Infarction recently published updated guidelines for the clinical and research diagnosis of myocardial infarction under a variety of circumstances and in a variety of categories. A type 1 myocardial infarction (MI) is usually the result of atherosclerotic coronary artery disease with thrombotic coronary arterial obstruction secondary to atherosclerotic plaque rupture, ulceration, fissuring, or dissection, causing coronary arterial obstruction with resultant myocardial ischemia and necrosis. Patients with a type 2 MI do not have atherosclerotic plaque rupture. In this latter group of patients, myocardial necrosis occurs because of an increase in myocardial oxygen demand or a decrease in myocardial blood flow. Type 2 MI has been the subject of considerable clinical discussion and confusion. This review by knowledgeable members of the Task Force seeks to help clinicians resolve the confusion surrounding type 2 MI.