Clinical Predictors of Incomplete ST-Segment Resolution in the Patients With Acute ST Segment Elevation Myocardial Infarction

BACKGROUND AND OBJECTIVES: The failure of ST-segment resolution (STR) after primary percutaneous coronary intervention (pPCI) is associated with adverse clinical outcomes. However, the clinical predictors on admission for incomplete STR are poorly known. SUBJECTS AND METHODS: Patients undergoing pPCI (n=101, 79 males and 22 females, mean age 60.0 years) were divided into complete STR group (> or =70%, n=58) and incomplete STR group (<70%, n=43). The groups were compared according to clinical factors including history, electrocardiographic (ECG) patterns, angiographic features and laboratory data. RESULTS: The incomplete STR group contained more frequent hypertensive patients (p=0.04) and patients displaying longer tendency in total chest pain duration (p=0.08). This group was associated with worse clinical factors such as low ejection fraction (p=0.06), higher Killip class (p=0.08) and more death (p=0.042). Grade 3 ischemia pattern of ECG and precordial ST elevation (i,e anterior myocardial infarction) at admission were more frequent in the incomplete STR group (p=0.001 and 0.002, respectively). Initial troponin I, creatinin kinase -MB and brain natriuretic peptide levels were higher in the incomplete STR group (p=0.001, 0.002, and 0.043, respectively). Coronary angiography showed that culprit lesions were more frequent in left anterior descending artery than other arteries in the incomplete STR group of patients (p=0.002). Thrombolysis In Myocardial Infarction (TIMI) flow grades 2 or less before PCI was more frequent in the incomplete STR group (p=0.029). However, TIMI flow grade after PCI was not appreciably different between the two groups. Logistic regression analysis demonstrated that TIMI flow grade 2 or less was most powerful predictor for incomplete STR {odds ratio (OR)=12.12, 95% confidence interval (CI) 1.23-119.35, p=0.032}. Other independent predictors were anterior infarction (OR=3.39, CI 1.46-10.57, p=0.007), ischemia grade 3 ECG at admission (OR=3.87, CI 1.31-11.41, p=0.014), and hypertensive patients (OR=3.03, CI 1.13-8.15, p=0.027). CONCLUSION: Incomplete STR after pPCI is associated with poor prognostic clinical factors. TIMI flow grade 2 or less before pPCI, ST elevation on precordial leads, ischemia grade 3 pattern of initial ECG, and hypertensive patients are independent predictors for incomplete STR in the early stage.

Carotid artery remodeling in patients with acute coronary syndrome and chronic stable angina / 대한내과학회지

BACKGROUND: Acute adaptive vascular remodeling occurs in active and unstable inflammatory plaques. It has been suggested that the adaptive coronary vascular remodeling, in patients with acute coronary syndrome (ACS), may be systemic and may show similar vascular remodeling in the carotid arteries. We investigated the ultrasonographic features of the common carotid artery (CCA) to determine whether the arterial expansive remodeling found in the coronary artery occurs in the carotid arteries of patients with ACS. METHODS: We measured lumen diameter (LD), interadventitial diameter (IAD) and intima media thickness (IMT) using a B-mode ultrasound in both common carotid arteries in patients with ACS (N=74) and chronic stable angina (CSA) (N=31). Positive remodeling was arbitrarily defined as an IMTmax >1 mm and IAD >8 mm and negative remodeling as an IMTmax >1 mm and IAD <7 mm. Other values were defined as "no remodeling" RESULTS: There were no significant differences in LD IAD and maximal IMT of the right CCA and the left CCA in comparisons between the ACS and the CSA patient groups. There were no differences for number of cases with no remodeling or differences in positive and negative remodeling in the right common carotid artery and left common carotid artery in comparisons between the ACS and CSA patient groups. . Presence of plaque in both common carotid arteries showed similar frequency in the ACS and CSA patient groups. The characteristics of carotid artery plaques were not different in the two groups. The remodeling index (IAD/LD) was correlated with IMTmax (right CCA r=0.797, p<0.001; left CCA r=0.860, p<0.001). CONCLUSIONS: The common carotid arterial structure of ACS patients was not different from that of CSA patients. Therefore, these results suggest that the expansive arterial remodeling, due to coronary inflammatory plaques, appears to take place locally rather than systemically.

A Case of Shoshin Beriberi Presenting as Acute Coronary Syndrome with Shock: Shoshin Beriberi Mimicking Acute Coronary Syndrome

Cardiac beriberi is caused by thiamine deficiency. Shoshin beriberi is a rare and fulminant form of cardiac beriberi characterized by hypotension, high output heart failure, lactic acidosis and anuria. Without early recognition and immediate treatment, most of these patients will be fatal. Therefore clinical diagnosis of shoshin beriberi is most important in emergency situation. We report a case of shoshin beriberi with clinical features mimicking acute coronary syndrome. Fifty year old male patient with chronic alcoholism was presented with shock, hypoxia, right heart failure and severe acidosis. Electrocardiogram showed abnormal Q in V1-3 and mild ST elevation and level of troponin I was slightly elevated. All manifestations including lactic acidosis were dramatically subsided in 18 hours by thiamine infusion. Even in developed country, shoshin beriberi can be occurred in patients with malnutrition and/or chronic alcoholism and should be differentiated with acute coronary syndrome.

A Case of Left Ventricular Pseudoaneurysm Extending to Lateral Side of Left Atrium after Myocardial Infarction

Left ventricular pseudoaneurysm is a rare but fatal complication of acute myocardial infarction. It occurs as a consequence of rupture of the ventricular free wall and is confined by a portion of pericardium. The pseudoaneurysm extended to lateral side of the left atrium is rare. We report a case of left ventricular pseudoaneurysm extended to lateral side of the left atrium in a 83-year-old man.