National Assessment of Statin Therapy in Patients Hospitalized with Acute Myocardial Infarction: Insight from China PEACE-Retrospective AMI Study, 2001, 2006, 2011

BackgroundStatin therapy is among the most effective treatments to improve short- and long-term mortality after acute myocardial infarction. The use of statin, and the intensity of their use, has not been described in acute myocardial infarction patients in China, a country with a rapidly growing burden of cardiovascular disease.ConclusionsThe use of statin therapy has dramatically increased over the past decade in Chinese patients with acute myocardial infarction. However, half of patients still did not receive intensive statin therapy in 2011.Given that guidelines strongly endorse intensive statin therapy for acute myocardial infarction patients, initiatives promoting the use of statin therapy, with attention to treatment intensity, would support further improvements in practice.     

Multivessel coronary thrombosis secondary to cocaine use successfully treated with multivessel primary angioplasty

Cocaine use has been associated with a significant risk of myocardial ischemia and myocardial infarction (MI). The previous approach to the treatment of cocaine-induced MI focused on medical treatment with verapamil, nitroglycerine and thrombolytics. Percutaneous revascularization for the cocaine-associated MI has been reported and is the preferred treatment modality. Identification of culprit vessel in the patients presenting with acute myocardial infarction associated with cocaine use is problematic owing to the frequent presence of baseline electrocardiogram (ECG) changes. Chronic cocaine use predisposes to diffuse coronary vasculopathy and may cause systemic alteration of coagulation parameters. Multivessel coronary thrombosis presenting as myocardial infarction associated with cocaine use has not been previously reported. This study describes a case of multivessel coronary thrombosis caused by cocaine ingestion successfully treated with multivessel primary angioplasty.     

A comparison of the illness beliefs of people with angina and their peers: a questionnaire study

Background

Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation.

Case presentation

A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI). Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints.

Conclusions

Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.     

Matrix metalloproteinases and membrane damage markers in sera of patients with acute myocardial infarction

Coronary artery disease is a multifunctional disease and represents one of the leading causes of death worldwide. Oxidative stress appears as an etiological factor for myocardial damage during acute myocardial infarction. Some data suggest that acute coronary syndromes may also be influenced by matrix metalloproteinases through degradation of the fibrous cap of vulnerable atherosclerotic lesions. It has been indicated that gelatinases A and B play a key role in acute myocardial infarction and deoxyribonuclease I has been postulated to be a novel early phase marker of disease. The aim was to study activity of gelatinases A and B in acute myocardial infarction and its association with some membrane damage markers. Seventy-five patients with disease and seventy-five healthy controls were enrolled. Activities of lactate dehydrogenase, malate dehydrogenase, and deoxyribonuclease I were estimated using standard spectrophotometric assay and isoforms of lactate and malate dehydrogenases were determined using direct zymography. Activity of dehydrogenases was significantly higher in patients, while deoxyribonuclease I was lower. Isoform 2 of lactate dehydrogenase was significantly higher in the patient group. Gelatinases A and B were detected only in patients group. The results suggest determination of serum malate dehydrogenase activity to be used as an additional parameter for acute myocardial infarction diagnosis. Those findings suggest important role of gelatinases A and B as biomarkers of early stage of acute myocardial infarction together with membrane damage parameters.     

急性心肌梗死患者肠道优势菌群分析

目的探讨急性心肌梗死患者肠道优势菌群的改变及其与疾病严重程度的关系。方法共筛选急性心肌梗死患者71名及正常健康体检者33名,急性心肌梗死患者根据是否心衰分为急性心肌梗死组36名和急性心肌梗死伴泵衰竭组35名,所有入选者收集大便及血清标本,分别采用qPCR及化学发光仪测定肠道优势菌群改变和血清脑钠肽前体及肌钙蛋白水平。结果急性心肌梗死患者肠道优势菌群显著改变,肠道肠杆菌以及肠球菌细菌数量较对照组显著增加,均与脑钠肽前体、肌钙蛋白、Killip分级显著正相关,而双歧杆菌、乳酸杆菌等细菌数量显著降低,与脑钠肽前体、肌钙蛋白、Killip分级显著负相关。结论急性心肌梗死患者呈现典型的肠道菌群紊乱,且与患者疾病严重程度相关。     

Morphological aspects of apoptosis in heart diseases

It has been suggested that apoptosis may be responsible for a significant amount of cardiomyocyte death during acute myocardial infarction as well as for a progressive loss of surviving cells in failing hearts. Typical apoptosis can indeed be induced in cardiomyocytes at the experimental conditions. In actual heart diseases, in contrast, there is very little direct morphological evidence of apoptosis in cardiomyocytes occurring at any stage of myocardial infarction and heart failure, despite the availability of much indirect evidence that includes detection of DNA fragmentation and apoptosis-related factors. For that reason, the potential efficacy of therapeutic intervention to prevent apoptosis remains controversial. This review will survey available data from both animals and humans to critically assess the role of cardiomyocyte apoptosis during myocardial infarction and its relevance to myocardial remodeling and during progression to heart failure. Also considered will be nonmyocyte interstitial cells, which have received less attention than myocytes despite definitive evidence of their apoptosis in the infarcted heart and recent studies suggesting that blockade of apoptosis among these cells mitigates postinfarction cardiac remodeling and heart failure. We conclude from our survey that there are many hurdles to surmount before regulation of apoptosis can be clinically applied in the treatment of myocardial infarction and heart failure.     

Mobile Intensive Care in Myocardial Infarction

In the first six months of its existence a mobile intensive care unit was used to admit 95 patients with definite or probable myocardial infarction to the local district hospital. Though the area served was a rural one, with a radius of about 25 miles from the hospital, the average interval between receiving a call and starting intensive care was less than 30 minutes. Five patients with ventricular fibrillation were successfully resuscitated by the mobile team outside hospital. The mobile unit has made it possible to admit many more patients with myocardial infarction to hospital than before, and we believe its cost and use of skilled staff are justified by the results. The unit reduces the delay between the onset of symptoms and initiation of intensive care and thus diminishes the risk of primary ventricular fibrillation, which is maximal soon after the onset of symptoms. Since mobile intensive care removes the risk of transport it allows concentration of cases of acute myocardial infarction in the larger hospitals.     

Myocardial infarction size: measurement and modification

The majority of in-hospital deaths from acute myocardial infarction occur as a result of the “power failure” syndrome (severe congestive heart failure and cardiogenic shock), which results from extensive loss of myocardium. The death of myocardial cells is sequential over many hours. Surrounding the central zone of necrosis in an acute myocardial infarction is a zone of ischemic myocardium whose fate might be altered by interventions during the early phase of the infarction. ST-segment mapping, serial measurement of the serum concentration of creatine phosphokinase and myocardial imaging by means of radionuclides are being developed for the noninvasive assessment of infarct size in animals and humans. A number of interventions appear to limit infarct size in animals. There have been relatively few studies in humans to date, but preliminary results suggest that infarct size might be limited by certain interventions. The research has provided important practical benefits in terms of understanding the course of acute myocardial infarction and the potential effects of conventional therapies. For the present, interventions designed to limit infarct size remain in the realm of clinical research; routine clinical use would be inappropriate.     

ANTICOAGULANT DRUG TREATMENT OF CORONARY ARTERY DISEASE

Anticoagulant therapy of arteriosclerotic heart disease may prove to be most valuable when applied on a long-term basis for prevention of recurrent myocardial infarction. While its prophylactic value in impending infarction has not been established, at least the accepted treatment for the acute stage is already begun if an anticoagulant has been administered before an inevitable infarction occurs.The chief value of the anticoagulant, though, seems to lie in preventing cardiac mural thrombosis and extracardiac thromboembolism. It is by this effect, apparently, that mortality has been reduced by 50 per cent among survivors of myocardial infarction who receive continuous dicoumarin therapy.While the danger of hemorrhage is still present, it is being steadily reduced by increasing skill in the management of anticoagulant therapy, and for a long time the risk has been far outweighed by the reduction in coronary occlusion.Physicians have a duty to learn the use of anticoagulant therapy, obtain the facilities necessary for it, and apply it to patients who are able and willing to cooperate in prolonging their useful lives.     

Light/dark patterns of interleukin-6 in relation to the pineal hormone melatonin in patients with acute myocardial infarction

AIMS: Atherosclerosis is a chronic disease that, from its origin to its ultimate complications, involves inflammatory cells, inflammatory proteins, and inflammatory responses from vascular cells. It has been demonstrated that cytokine activities are under neuroendocrine control, in part exerted by the pineal gland through the circadian secretion of its main product melatonin. Melatonin is mainly released during the night, but the precise relationship between melatonin and the light/dark rhythm of interleukin-6 in patients with acute myocardial infarction is still unclear. METHODS AND RESULTS: The study included 60 patients diagnosed with acute myocardial infarction and 60 healthy volunteers whose venous blood samples were collected at 09:00 h (light period) and 02:00 h (dark period). Our results demonstrate that interleukin-6 concentrations presented a light/dark pattern with mean serum concentrations being higher in the acute myocardial infarction group than in the control group (101.26 +/- 13.43 and 52.67 +/- 7.73 pg/ml at 02:00 h, 41.93 +/- 5.90 and 22.98 +/- 4.49 pg/ml at 09:00 h, respectively, p < 0.05). Differences in the day/night changes in melatonin levels in control subjects (48.19 +/- 7.82 at 02:00 h, 14.51+/- 2.36 at 09:00 h, pg/ml) and acute myocardial infarction patients (25.97 +/- 3.90 at 02:00 h, 12.29 +/- 4.01 at 09:00 h, pg/ml) (p < 0.05) were a result of a reduced nocturnal elevation of melatonin in the acute myocardial infarction group. CONCLUSIONS: The current findings suggest that the circadian secretion of melatonin may be responsible at least in part for light/dark variations of endogenous interleukin-6 production in patients with acute myocardial infarction. In this study, the melatonin seems to have an anti-inflammatory effect.     

Effect of obsidan on metabolic processes in the blood and lymph in acute myocardial infarction

The effects of obsidan on lactate and glucose levels, the indices of ABB and electrolyte metabolism in blood and lymph at various times after development of the acute myocardial infarction were studied experimentally on dogs. It was stated that the earliest and most expressed changes of biochemical values were observed in the lymphatic system, thus pointing to its important role in the resorption and transport of the metabolic products from ischaemic myocardium. The use of obsidan during the development of acute myocardial infarction corrects substantially the disturbed metabolic processes in the blood and lymph.     

General practitioners' management of acute myocardial infarction and cardiac arrest: relevance to thrombolytic treatment.

A questionnaire was sent to 61 general practitioners who had participated 18 months previously in a study of their experience of cardiopulmonary resuscitation and defibrillation in acute myocardial infarction. Fifty (82%) replies were received. Only 16 of the 50 respondents thought that every general practitioner should have a defibrillator, but 46 thought that every group practice should have one. Most practitioners felt the need for more tuition and practice in advanced life support, but 15 did not have the practice defibrillator with them when on call. Only nine doctors normally had an electrocardiograph with them when on call, most relying on clinical acumen to make an operational diagnosis; there appeared to be reluctance to use any drugs other than opiates and atropine in the management of acute myocardial infarction. This study highlights the difficulty of maintaining readiness to deal effectively with myocardial infarction in the community and the problems of relying on the electrocardiogram in deciding who should be given thrombolytic treatment.     

Management of patients after their first myocardial infarction.

In the past 20 years there has been a steady improvement in the short term prognosis of patients with myocardial infarction, following the introduction of beta blockers, thrombolysis, and aspirin. Patients treated with thrombolytic drugs have a lower overall mortality after myocardial infarction but remain at risk of non-fatal reinfarction or death, and in one study almost half of all survivors of acute myocardial infarction died or suffered a further ischaemic event within three years. It is therefore important to have a strategy to identify patients at high risk, to reduce the subsequent development of cardiac failure and mortality, and to have effective measures for secondary prevention to reduce the incidence of reinfarction as well as to promote rehabilitation.     

Acute Myocardial Infarction: Clinical Application of Technetium 99m Stannous Pyrophosphate Infarct Scintigraphy

Acute myocardial infarction is being recognized as a spectrum of clinical subsets. This appreciation has been brought about to a large degree by the development of several new tools that can be applied clinically to aid in evaluation of patients with acute infarction, and in some cases to provide short and long-term prognostic information. In the realm of noninvasive methods, several tests utilizing radiopharmaceuticals and scintillation cameras have emerged and are rapidly becoming reliable diagnostic parameters in patients with coronary disease and infarction. Technetium 99m (stannous) pyrophosphate (TcPYP) scintigraphy, one of the first of these techniques to find clinical use, has been shown to be an accurate indicator of acute transmural myocardial infarction and provides added sensitivity and specificity to the diagnosis. Increased diagnostic accuracy, the dimension of visible localization and the potential for infarct sizing promise physicians better understanding of a patient''s clinical presentation and a more rational approach to management.     

Paroxysmal atrial fibrillation triggered by a monomorphic ventricular couplet in a patient with acute coronary syndrome

Atrial fibrillation is a common arrhythmia in patients suffering from acute myocardial infarction, however its pathophysiological mechanisms are not fully understood. We describe the unusual case of a 76-year old woman admitted for non-ST-segment elevation myocardial infarction, who developed multiple episodes of paroxysmal atrial fibrillation triggered by monomorphic ventricular couplets. Beta-blocking and amiodarone therapy resulted efficacious in preventing arrhythmic recurrences. We then discuss the possible arrhythmogenic mechanisms, with special emphasis on the unique electrophysiological, hemodynamic, cellular and anatomical milieu created by acute myocardial ischemia.     

Dipyridamole: a Controlled Trial of its Effect in Acute Myocardial Infarction

A controlled trial of oral dipyridamole in 103 patients with acute myocardial infarction showed no difference in the number of complications or deaths in either the control or the treated groups. It is concluded that dipyridamole has no benefit in acute myocardial infarction.     

Prognostic significance of acute systolic hypertension after myocardial infarction.

The clinical behaviour and mean peak serum aspartate aminotransferase (SGOT) values of 106 patients admitted to a coronary care unit with acute myocardial infarction who displayed acute systolic hypertension were studied. Another 106 normotensive patients with acute myocardial infarction acted as controls. Neither group had established hypertension. The mortality rate, incidence of cardiac failure, major arrhythmias, and mean peak SGOT were significantly greater in the hypertensive group, within which the duration of hypertension was correlated with mean peak SGOT levels--through there was no definite relation between the height of systolic or diastolic pressure and SGOT. Transient systolic hypertension after acute myocardial infarction was therefore associated with a relatively poor prognosis, but our observations suggest that patients with a systolic blood pressure of at least 170 mm Hg might benefit from early hypotensive treatment.     

Initial Heparin Therapy in Acute Myocardial Infarction

The administration of heparin during the first 48 hours following acute myocardial infarction is widely practised. Heparin treatment is also recommended for acute coronary insufficiency on the grounds that it may prevent development of an impending myocardial infarction. These measures had been accepted without support of a controlled clinical trial. By random selection, 101 patients hospitalized with a provisional diagnosis of acute myocardial infarction received heparin (100 mg. intravenously every eight hours for 48 hours) and 105 patients were assigned to a control group. Both groups of patients received bishydroxycoumarin (Dicumarol). The mortality in the heparin series was 30% and in the control group, 28%. A significantly large number of the heparin-treated patients developed clinical and laboratory proof of recent myocardial infarction. It is concluded that early intermittent intravenous heparin treatment does not lower the mortality in patients with acute myocardial infarction nor does it prevent impending myocardial infarction in patients with acute coronary insufficiency.     

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

     

Therapeutic application of ultrasound: contrast-enhanced thrombolysis in acute ST-elevation myocardial infarction; the Sonolysis study

Contrast enhancement by microbubble infusion has proven its applicability in the field of diagnostic ultrasound. Recent studies also indicate a therapeutic effect of the combined use of ultrasound and microbubbles. Results from animal studies demonstrate that diagnostic ultrasound in combination with intravenous microbubbles can dissolve thrombi. So far, this effect has never been tested in patients with an acute ST-elevation myocardial infarction (STEMI). We recently launched a pilot study in acute STEMI patients to assess safety, feasibility and efficacy of the treatment in this patient group with transthoracic three-dimensional diagnostic ultrasound and intravenous microbubbles immediately after prehospital thrombolysis, but prior to primary percutaneous coronary intervention.