The exact etiology of the coronary slow flow phenomenon (CSFP) is not certain. CSFP is not a normal variant as it is an absolutely pathological entity. Furthermore, CSFP not only leads to myocardial ischemia but it can also cause classical acute ST elevation myocardial infarction, which necessitates coronary angiography for a definite diagnosis.
Anterior Wall Myocardial Infarction ; Coronary Angiography ; Myocardial Infarction ; Myocardial Ischemia ; No-Reflow Phenomenon

BACKGROUND: Left ventricular thrombus is a common complication after acute myocardial infarction. Methods and RESULTS: To Study the incidence of left ventricular thrombosis (LVT) after acute myocardial infarction, we performed serial two-dimensional echocardiography (2D-Echo) in 35 consecutive patients with acute myocardial infarction prospectively ; 10 patients had inferior wall myocardial infarction, 25 patients had anterior wall myocardial infarction. 2D-Echo was obtained within 3 days of acute myocardial infarction, at 4-10 days after symptom onset, and 2-4 weeks after symptom onset serially in each case. 19 out of 35 patients received thrombolytic therapy with urokinase. Left ventricular thrombi were identified in 9(25.7%) of the 35 study patients. The location of myocardial infarction was anterior and apical in all cases with left ventricular thrombi. The shape of thrombi was mural in 6 cases and protruding in 3 cases. The incidence of left ventricular thrombi in patients who received urokinase was not significantly different from that in patients who didn't(31.9% vs 18.8%,p=0.22). Wall motion score was significantly higher in patients who developed left ventricular thrombi than in patients who had no left ventricular thrombus(8.2+/-1.9 vs 5.8+/-2.6, p<0.005). All thrombi appeared within 10 days after myocardial infarction. CONCLUSIONS: Thus left ventricular thrombi develops within 10 days following myocardial infarction with large anterior and apical location. The thrombolysis therapy has no effect in the incidence of left ventricular thrombi in this study. But because of confounding effect of thrombolysis and location of myocardial infarction and extent of myocardial infarction, further investigation is needed.
Anterior Wall Myocardial Infarction ; Echocardiography ; Humans ; Incidence* ; Inferior Wall Myocardial Infarction ; Myocardial Infarction* ; Prospective Studies ; Thrombolytic Therapy ; Thrombosis* ; Urokinase-Type Plasminogen Activator

The incidence of acute myocardial infarction (AMI) is increasing. Acute papillary muscle rupture is one of the serious and rare mechanical complications of AMI, which occurs mostly in inferior and posterior myocardial infarction. A patient with acute inferior myocardial infarction developed pulmonary edema and refractory shock, followed by cardiac arrest. After cardiopulmonary resuscitation (CPR), revascularization of criminal vessels was carried out by emergency percutaneous transluminal coronary angioplasty (PTCA) under the support of intra-aortic balloon pump (IABP) and extra corporeal membrane oxygenation (ECMO). Although the patient was given a chance for surgery, his family gave up treatment due to unsuccessful brain resuscitation. It reminds that mechanical complications such as acute papillary muscle rupture, valvular dysfunction and rupture of the heart should be highly suspected when cardiogenic pulmonary edema and cardiogenic shock are difficult to correct in acute inferior myocardial infarction. Echocardiogram and surgery should be put forward when revascularization of criminal vessels is available.
Humans ; Inferior Wall Myocardial Infarction/complications* ; Papillary Muscles/surgery* ; Pulmonary Edema ; Myocardial Infarction/surgery* ; Shock, Cardiogenic

No abstract available.
Electrocardiography* ; Inferior Wall Myocardial Infarction*

A 63 year old male suffered from a acute huge inferolateral and posterior myocardial infarction with vertricular septal perforation(1x1.5cm). Cardiogenic shock and ventricular tachycardia occured on the 3rd day in hospital. After cardiopulmonary resuscitation the deteriorated condition of the patient was improved by intraaortic balloon counterpulsation(IABP). The invasive diagnostic procedure(LV angiography and coronary angiogram) was carried out under the employment of IABP and artificial ventrilation. The patients has recovered from the operation(coronary artery bypass graft and VSD patch op) and myocardial infarction. Because of recurrent aspiration pneumonia the patient was nourished per gastrostomy. He died 3 month later due to upper gastrointestinal bleeding.
Angiography ; Arteries ; Cardiopulmonary Resuscitation ; Counterpulsation* ; Employment ; Gastrostomy ; Hemorrhage ; Humans ; Inferior Wall Myocardial Infarction* ; Male ; Middle Aged ; Myocardial Infarction ; Pneumonia, Aspiration ; Shock, Cardiogenic* ; Tachycardia, Ventricular ; Transplants ; Ventricular Septal Rupture*

OBJECTIVETo investigate the impact of pre-primary percutaneous coronary intervention (PCI) β blocker use on the development of no-reflow in ST-segment elevation myocardial infarction (STEMI) patients post PCI.

METHODSWe retrospectively evaluated 1 615 outpatients with STEMI who underwent primary primary PCI with in 12 hours from symptom onset admitted to Beijing Anzhen Hospital and Chinese people's liberation army general hospital from January 2007 to June 2011. The study population was divided into the following 2 groups: β blocker group (pretreatment with β blockers ≥ one month before admission, n = 257) and non-β blockers group (pretreatment with β blockers < one month before admission or had no β blocker, n = 1 358). No-reflow was defined as TIMI grade < 3 in last imaging of coronary artery after stenting. Multivariable logistic regression analyses were used to identify independent predictors for the no-reflow after primary PCI.

RESULTSIncidence of the no-reflow was significantly lower in the β blocker group than in non-β blockers group (13.6% (35/257) vs. 21.2% (289/1 358), P = 0.017). Multivariable logistic regression analysis revealed that pre-PCI β blocker use was a protective predictor of the no-reflow (OR = 0.594, 95%CI:0.394-0.893, P = 0.012), while age ≥ 55 years old (OR = 2.734, 95%CI:1.959-3.817, P < 0.001), high neutrophil count (OR = 1.257, 95%CI: 1.169-1.351, P < 0.001), admission plasma glucose (OR = 1.060, 95%CI:1.018-1.103, P = 0.004), Killip classes IV (OR = 3.383, 95%CI:1.924-5.948, P < 0.001) and reperfusion time ≥ 4 h(OR = 1.503, 95%CI:1.124-2.009, P = 0.006) were risk factors for the development of no-reflow post PCI.

CONCLUSIONPrevious long term β blockers use before STEMI is associated with lower incidence of no-reflow in patients with STEMI treated with primary PCI.

Adrenergic beta-Antagonists ; therapeutic use ; Aged ; Angioplasty, Balloon, Coronary ; Anterior Wall Myocardial Infarction ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention ; Retrospective Studies ; Risk Factors ; Stents

BACKGROUND AND OBJECTIVES: Dual blood supply to the anterior interventricular septum (IVS), derived from the septal branches of the left anterior descending artery (LAD) and the conal branch of the right coronary artery (RCA), may prevent ST segment elevation in lead V1 during an anterior acute myocardial infarction (AMI), and predict a favorable in-hospital clinical course. SUBJECTS AND METHODS: The admission 12-lead electrocardiogram (ECG), and the coronary angiograms performed within 10 days of hospital admission, were evaluated in 67 patients with anterior wall AMI, as defined by a ST segment elevation > or =2mm in at least 2 of the V1 to 4 leads. The patients were divided into two groups according to the magnitude of the ST segment elevation in V1 lead: group 1 (ST <1.5 mm, n=22) and group 2 (ST > or =1.5 mm, n=45). The conal branch types were classified into small (a diameter <0.5 mm), not reaching the IVS, and large (a diameter >0.5 mm), reaching the IVS. RESULTS: A large conal branch was found in 11 patients of each group 50 and 24%, respectively (p=0.04). There was no significant relation between the sites of the LAD lesion, whether proximal or distal to the first septal branch, and the presence of ST segment elevation in lead V1. The serum cardiac enzymes, Killip class and the incidence of in-hospital congestive heart failure, were not significantly different. CONCLUSION: The absence of ST segment elevation in lead V1 during an anterior AMI suggested that the IVS is protected by a large conal branch, in addition to the septal branch of the LAD, but this did not influence the in-hospital clinical course.
Anterior Wall Myocardial Infarction* ; Arteries ; Coronary Vessels* ; Electrocardiography ; Heart Failure ; Humans ; Incidence ; Myocardial Infarction ; Prognosis

The de Winter electrocardiogram pattern is an acute ST-segment elevation myocardial infarction equivalent, however this specific electrocardiogram change is easily ignored by clinicians. The de Winter electrocardiogram pattern in patients with acute chest pain mostly indicates sub-complete or complete occlusion of the left anterior descending or the diagonal branch. Patients with acute chest pain and such electrocardiographic finding should undergo emergency coronary angiography immediately to determine the coronary condition, and reperfusion therapy should be performed as soon as possible to reduce the incidence of adverse cardiovascular events.
Anterior Wall Myocardial Infarction ; Cognition ; Coronary Angiography ; Electrocardiography ; Humans ; ST Elevation Myocardial Infarction/diagnosis*

BACKGROUND AND OBJECTIVES: Acute myocardial infarction-related heart failure (HF) is associated with poor outcome. This study was designed to investigate the usefulness of global longitudinal strain (GLS), global circumferential strain (GCS) and mean longitudinal strain of left anterior descending artery territory (LSant) measured by 2-dimensional speckle tracking echocardiography (2D STE) in prediction of acute anterior wall ST-segment elevation myocardial infarction (ant-STEMI)-related HF. METHODS: A total of 171 patients with ant-STEMI who underwent successful primary coronary intervention and had available 2D STE data were enrolled. Patients were divided into 3 groups: in-hospital HF, post-discharge HF, and no-HF groups. RESULTS: In-hospital and post-discharge HF developed in 39 (22.8%) and 13 (7.6%) of patients, respectively and 113 patients (69.6%) remained without HF. Multivariate analysis showed that GLS was the only factor significantly associated with the development of in-hospital HF. For post-discharge HF, LSant was the only independent predictor. Other echocardiographic or laboratory parameters did not show independent association with the development of ant-STEMI-related HF. CONCLUSIONS: GLS is a powerful echocardiographic parameter related to development of in-hospital HF and LSant was significantly associated with post-discharge HF in patients with successfully reperfused ant-STEMI.
Anterior Wall Myocardial Infarction ; Arteries ; Echocardiography ; Heart Failure ; Heart ; Humans ; Multivariate Analysis ; Myocardial Infarction

BACKGROUND: Unstable angina is a critical phase of ischemic heart disease, but there are no reliable noninvasive methods of assigning patients to different prognostic actegories. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial injury. We investigated the value of the Troponin-T in unstable angina to determine whether the increase of cardiac Troponin-T might be a useful predictor of prognosis. METHODS: Unstable angina is defined as Braunwald classification(Class I, II, III). CLass I is new onset of severe angina or accelerated angina and no rest pain, class II is angina at rest but not within preceding 48 hour, and class III is angina at rest within 48 hour. We studied 16 cases of unstable angina(male:10, mean age:57+/-2year). We measured Troponin-T and CK-MB at admission, after 6 hours, and every 8 hour for 2 days. For the determination of serum Troponin-T, an enzyme immunosorbent assay (Boehringer Mannheim, ES 300 analyzer) was used. Above 0.1ng/ml was regarded as positive. During the admission, we investigated the myocardial infartion, sudden death, and the need of emergency PTCA and CABG. RESULTS: 1) Among 16 unstable angina patients, there are 12 patients in Class I(range 0.001-0.13, mean SD 0.04 0.01, median 0.02ng/ml) and 4 patients in Class III(range 0.03-1.56, mean SD 0.39 0.2, median 0.27ng/ml) and 4 patients showed positive value of Troponin-T. One was in Class I and the others were in Class III. 2) During the admission, one patient expired due to cardiogenic shock preceding inferior myocardial infarction, and 2 patients progressed non-Q wave myocardial infarction(NQMI). These 3 patients were in unstable angina Class III and had positive Troponin-T value. In Class I, one patient performed emergency CABG due to consistent chest pain at the sixth hospital day. These patient had negative Troponin-T value. 3) CK-MB increased in one patient with NQMI, and the other patients were not increased. CONCLUSION: Cardiac Troponin-T in serum appears to be a more sensitive indicator of myocardial cell injury than serum creatine Kinase MD activity, and its detection in the circulation may be a useful porgnostic indicator in patients with unstable angina.
Angina, Unstable* ; Chest Pain ; Creatine Kinase ; Death, Sudden ; Emergencies ; Humans ; Inferior Wall Myocardial Infarction ; Myocardial Ischemia ; Prognosis ; Shock, Cardiogenic ; Troponin T*