Electrocardiographic differentiation between acute pulmonary embolism and non-ST elevation acute coronary syndromes at the bedside.

BACKGROUND: Clinical picture of acute pulmonary embolism (APE), with wide range of electrocardiographic (ECG) abnormalities can mimic acute coronary syndromes. OBJECTIVES: Assessment of standard 12-lead ECG usefulness in differentiation at the bedside between APE and non-ST elevation acute coronary syndrome (NSTE-ACS). METHODS: Retrospective analysis of 143 patients: 98 consecutive patients (mean age 63.4 +/- 19.4 year, 45 M) with APE and 45 consecutive patients (mean age 72.8 +/- 10.8 year, 44 M) with NSTE-ACS. Standard ECGs recorded on admission were compared in separated groups. RESULTS: Right bundle branch block (RBBB) and S(1)S(2)S(3) or S(1)Q(3)T(3) pattern were found in similar frequency in both groups (10 [11%] APE patients vs 6 [14%] NSTE-ACS patients, 27 [28%] patients vs 7 [16%] patients, respectively, NS). Negative T waves in leads V(1-3) together with negative T waves in inferior wall leads II, III, aVF (OR 1.3 [1.14-1.68]) significantly indicated APE with a positive predictive value of 85% and specificity of 87%. However, counterclockwise axis rotation (OR 4.57 [2.74-7.61]), ventricular premature beats (OR 2.60 [1.60-4.19]), ST depression in leads V(1-3) (OR 2.25 [1.43-3.56]), and negative T waves in leads V(5-6) (OR 2.08 [1.31-3.29]) significantly predicted NSTE-ACS. CONCLUSIONS: RBBB, S(1)S(2)S(3), or S(1)Q(3)T(3) pattern described as characteristic for APE were not helpful in the differentiation between APE and NSTE-ACS in studied group. Coexistence of negative T waves in precordial leads V(1-3) and inferior wall leads may suggest APE diagnosis.

Is it possible to use standard electrocardiography for risk assessment of patients with pulmonary embolism?

BACKGROUND: Risk stratification of patients with acute pulmonary embolism (APE) is crucial for appropriate treatment selection. Shock and hypotonia are known indications for aggressive management. However, in the haemodynamically stable group the best prognosis strategy is still being sought. Acute pulmonary embolism often provokes changes in electrocardiography recordings (ECG). AIM: To assess whether ECG features recorded on admission can be useful for risk stratification during hospitalisation. METHODS: We analysed 12-lead ECG and echocardiography of 56 patients (22 males, age: 64.3 +/- 17.9 years) with diagnosed APE. The diagnosis of APE was confirmed by spiral computer tomography. The ECG analysis was based on the 21-point ECG score including: the presence of tachycardia (> 100 beats/min), right bundle branch block, negative S waves in lead I, negative Q or T waves in lead III, S1Q3T3 complex and depth of negative T waves in leads V1-V4. ECG features were scored from 0 to 21 points. Complicated in-hospital course was defined as need for vasopressor, thrombolysis, embolectomy or resuscitation and the presence of shock index > 1 (heart rate/systolic blood pressure). RESULTS: Four (7.1%) patients died during hospitalisation and in 8 (14.3%) others complications occurred. Patients with complications had higher mean sum of 21-ECG score compared to subjects with uneventful course [8 (1-17) vs. 3 (0-18); p = 0.04]. Right ventricular contractility dysfunction (RVD) in echocardiography was found in 13 (23.2%) patients, who had higher ECG score compared to patients without RVD [8 (3-17) vs. 2 (0-18); p = 0.004]. The area under the ROC curve to assess the usefulness of 21-ECG score to predict RVD was 0.794 (95% CI 0.665-0.891) and for PPH 0.727 (95% CI 0.591-0.837). The sensitivity and specificity, positive and negative predictive value for the value > 3 points in 21-ECG score to predict RVD were: 92, 65, 44, 97% and for PPH: 75, 46, 19, 92%, respectively. CONCLUSIONS: 21-ECG score is a simple and cheap method which can be used to predict RVD and serious complications in patients with APE. A value L 3 points in the 21-ECG score can exclude RVD with high probability and limit the need of echocardiography to 23% of haemodynamically stable patients.

Does time delay between the primary cardiac arrest and PCI affect outcome?

OBJECTIVES: In patients with acute ST-segment elevation acute myocardial infarction (AMI), no data are available on the prognostic value of cardiac arrest (CA) due to ventricular fibrillation (VF) before, during, and after percutaneous coronary intervention (PCI). The aim of our study was to determine differences in prognosis between patients with CA before, during, and after PCI. METHODS: Among 448 patients with first ST-segment elevation AMI, we selected 34 (7.6%) with primary CA due to VF and 6 (1.3%) with secondary CA. The patients with primary CA were categorized into groups according to the time of the first episode of the primary CA, either before [12 (35.3%)], during [18 (52.9%)], or after [4 (11.8%)] PCI procedure. The 30-day all-cause mortality rate was analysed. RESULTS: Short-term mortality was: (i) in patients without CA: 7.1% (29/408); (ii) in patients with primary CA 35.3% (12/34); (iii) in patients with secondary CA 50% (3/6); (P < 0.001). Mortality was 8.3% (1/12) in patients with primary CA before PCI; 44.4% (8/18) in patients with primary CA during PCI; 75% (3/4) in patients with primary CA after PCI procedure; (P = 0.007). CONCLUSIONS: Patients with a primary CA have the same poor prognosis as patients with a secondary CA. The prognosis worsened according to the time of the occurrence of the primary CA. It might be reasonable to isolate subgroups of ST-segment elevation AMI patients treated with PCI with primary CA according to time of primary CA. This could help to better stratify the risk of these patients.

Usefulness of myocardial necrosis triad markers for predicting 4-year mortality in patients with suspected acute coronary syndrome.

OBJECTIVE: Cardiac troponins (cTn), creatine kinase-MB (CK-MB), myoglobin (MYO) are commonly used biochemical markers for risk stratification and diagnosis in patients with suspected acute coronary syndrome (ACS). The aim of the study was to analyse the prognostic implications of 3 myocardial necrosis markers measured at admission in the long-term observation. METHODS: The study group consisted of 336 consecutive patients whose concentration of cTnl, CK-MB and MYO were measured at admission. Patients were categorized into 4 groups according to the number of positive myocardial necrosis markers. RESULTS: There was a significant increase in the mean marker levels with increasing numbers of positive markers (over upper normal range): cTnl (0.02 +/- 0.06; 0.7 +/- 1.9; 3.4 +/- 8.8; 5.1 +/- 9.2 ng/ml; P < 0.001), CK-MB (1.3 +/- 1.1; 3.3 +/- 3.9; 21.9 +/- 39.4; 37.5 +/- 48.4 ng/ml; P < 0.001), MYO (39.4 +/- 16.5; 94.5 +/- 91; 202.2 +/- 172.2; 320.3 +/- 234.3 ng/ml; P < 0.001). There was a statistically significant increase in the 4-year all-cause mortality with increasing numbers of positive markers; P value for trend < 0.0001. CONCLUSIONS: All 3 marker levels at admission may be an important addition to the risk stratification of patients with suspected ACS and a potentially important target for therapy. They have prognostic implications in the long-term observation of patients with chest pain and suspected ACS.

[Exudative pericarditis due to secondary kidney amyloidosis--a case report]. / Wysiekowe zapalenie osierdzia w przebiegu wtórnej amyloidozy nerek--opis przypadku.

Non-infective pericarditis in some cases may be caused by secondary amyloidosis. Amyloidosis is a metabolic disorder in which amyloid protein is deposited in various organs and destroys them. The most frequent location of systemic amyloidosis are the kidneys. In this case study we report a 74-year-old man who was admitted to hospital due to very poor condition, generalised oedema and severe dyspnoea. Since 2003 the patient had been hospitalised many times due to pericarditis of unknown aetiology. In this case we diagnosed exudative pericarditis due to nephrotic syndrome caused by secondary kidney amyloidosis which occurs very rarely.

Electrocardiographic features and prognosis in acute diagonal or marginal branch occlusion.

The aim of our study was to analyze electrocadiographic changes in patients with acute myocardial infarction related to the occlusion of diagonal (DG) or marginal (MG) branch. We selected 13 cases with DG and 12 with MG occlusion on angiography and evaluated their electrocardiogram (ECG) patterns on admission obtained in emergency department (ED) of university hospital with catheterization laboratory serving everyday interventional cardiology duty for ACS. Most characteristic ECG changes in acute occlusion of DG observed in 12 patients (92.3%) included ST-segment elevation in leads V(2) and V(3) (mean, 1.2 +/- 0.5 mm; maximum, 1.7 mm) and ST-segment depression in leads II and III (mean, 0.9 +/- 0.4 mm; maximum, 1.5 mm). Most characteristic ECG changes for acute occlusion of MG were ST-segment depression in leads V(5) and V(6) (mean, 0.9 +/- 0.4 mm; maximal, 1 mm) observed in 11 (91.7%) patients, ST-segment depression in lead II (mean, 0.7 +/- 0.2 mm; maximal, 0.8 mm) in 10 (83.3%,) and in leads V(2) and V(3), and aVF in 8 (66.7%) of cases. Risk of complications including cardiogenic shock and death was high in both groups especially during acute phase of myocardial infarction. Prevalence of borderline ECG changes in patients with acute coronary occlusion confirms how important is precise ECG interpretation usually initially done by ED physician.

Prognostic implications of myocardial necrosis triad markers' concentration measured at admission in patients with suspected acute coronary syndrome.

The aim of the study was to analyze the prognostic implications of 3 myocardial necrosis markers measured at admission in short-term observation of patients with suspected acute coronary syndrome. The study group consisted of 336 consecutive patients whose concentration of cardiac troponin I, creatine kinase-MB fraction, and myoglobin were measured at admission. All patients referred due to chest pain and suspected acute coronary syndrome and were followed up for 30 days. The patients who died had statistically higher concentration of cardiac troponin I (8.7 +/- 17.2 vs 0.9 +/- 3.2 ng/mL; P = .0006), myoglobin (215.2 +/- 181.5 vs 109.7 +/- 151.5 ng/mL; P = .003), and creatine kinase-MB (21.9 +/- 30.7 vs 8.8 +/- 25.9 ng/mL; P = .005), compared to patients who stayed alive. There was statistically significant increase in 30-day all-cause mortality with increasing numbers of positive markers-0.6% for patients with nonpositive marker, 3.4% for patients with 1 positive marker, and 11.5% for patients with at least 2 positive markers (P = .001 for trend).