Abdolhamid Sheikhzadeh

Aortic atherosclerotic plaques as a source of systemic embolism

OBJECTIVES Our study was designed to determined the significance of aortogenic embolism in an unselected autopsy collective. BACKGROUND Although embolism arising from atherosclerotic plaques in the aorta has been acknowledged, the role of aortic atheromatosis among other well known sources of embolism remains to be further clarified. METHODS We examined the proximal part of the arterial system with regard to the presence of atherosclerotic lesions as well as cardiac changes in 120 consecutive necropsy studies. Pathologic evidence of embolic events was recorded. Clinical and neuropathologic data were also surveyed in all patients. RESULTS Among atherosclerotic lesions, fibrous plaques (p < 0.05) and calcified (p < 0.0001) and ulcerated lesions (p < 0.0001) as well as thrombi (p < 0.005) were observed significantly more frequently in the aortic arch and in the descending aorta than in the ascending aorta, whereas fatty streaks were distributed uniformly. In 40 (33%) of the 120 patients, we found pathologic evidence of arterial embolization. Multiple logistic regression analysis revealed a significant correlation between embolism and complicated atherosclerotic plaques in the aortic arch (odds ratio [OR] 5.8, 95% confidence interval [CI] 1.1 to 31.7, p < 0.05), severe ipsilateral carotid artery disease (OR 3.1, 95% CI 3.1 to 45.3, p < 0.001) and atrial fibrillation (OR 3.5, 95% CI 1.1 to 9.9, p < 0.05). CONCLUSIONS Complicated atherosclerotic plaques in the aortic arch represent an independent risk factor for systemic embolism similar to atrial fibrillation and severe atherosclerosis of the carotid arteries.

Relation of left atrial appendage function to the duration and reversibility of nonvalvular atrial fibrillation

Transesophageal echocardiography provides a tool to assess the functional integrity of the LAA during AF. This is the first study to demonstrate an association between LAA mechanical function and the duration of AF, which can be defined before cardioversion is undertaken. A high level of LAA mechanical function during AF seems to indicate a potential reversibility of the arrhythmia, whereas a low level of LAA outflow velocities is associated with stasis and elevated thromboembolic risk.

Myocardial ischemia in generalized coronary artery–left ventricular microfistulae

Generalized (multiple) arterio-systemic fistulae are fistulae arising from all three major coronary arteries and drain into the left ventricle are rare and the clinical and hemodynamic sequelae are incompletely understood. This communication is based on the clinical and hemodynamic data of a series of patients (eight cases out of 7262 consecutive patients) incidentally identified at coronary angiography combined with data from cases previously reported in literature. The aim was to assess the role of generalized coronary artery fistulae as a non-atherosclerotic cause of myocardial ischemia by means of a coronary sinus lactate study. Coronary sinus lactate study demonstrated myocardial ischemia in 6/7 patients. Mean arterio-coronary venous lactate difference decreased from 0.31+/-0.18 mmol/l (lactate extraction ratio, LER, 29.4+/-13.9%) at rest to 0.04+/-0.13 mmol/l (LER -4.0+/-13.3%) at peak exercise. Five minutes after cessation of pacing, lactate difference increased to 0.22+/-0.21 mmol/l (LER -20.7+/- 13.2%). At peak pacing stress, 4/7 patients showed frank lactate production, and two patients presented with a reduced cardiac lactate extraction rate also indicating myocardial ischemia metabolically. In the present study, we demonstrated a possible role of a coronary steal mechanism due to microfistulae pathways in the pathogenesis of myocardial ischemia in patients with generalized coronary artery-left ventricular microfistulae.

Prothrombin fragments F1+2, thrombin–antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

Transesophageal echocardiographic determinants of embolism in nonrheumatic atrial fibrillation.

The purpose of the study was to determine the relation of transesophageal echocardiographic findings to symptoms of systemic embolism in patients with nonrheumatic atrial fibrillation. Transthoracic and transesophageal echocardiography were used to study 107 patients with atrial fibrillation including 49 patients without embolic complications and 58 patients who had suffered from previous cerebral or peripheral embolism. A multiple logistic regression analysis revealed that left atrial thrombi (odds ratio 9.0, 95% CI 2.4–33.6, p < 0.005) and the presence of dense left atrial spontaneous contrast (odds ratio 8.4, 95% CI 1.3–53.1, p < 0.05) were independently related to embolic symptoms. Intensive left atrial spontaneous contrast was associated with an increased left atrial diameter (odds ratio 2.0, 95% CI 1.1–3.6, p < 0.05), the presence of chronic atrial fibrillation (odds ratio 6.9, 95% CI 1.6–29.8, p < 0.01) and aortic atherosclerosis (odds ratio 2.6, 95% CI 1.2–5.5, p < 0.05). It was further negatively correlated to mitral regurgitation (odds ratio 0.4, 95% CI 0.2–0.9, p < 0.05). In conclusion, dense spontaneous echo contrast and left atrial thrombi are associated to thromboembolic complications in patients with nonrheumatic atrial fibrillation. Classifying of spontaneous contrast seems to be useful when estimating the thromboembolic risk in atrial fibrillation.

In-patient cardiac rehabilitation versus medical care – a prospective multicentre controlled 12 months follow-up in patients with coronary heart disease

Background: The aim of this study was to evaluate a 3-week inpatient cardiac rehabilitation (Rehab) started early after the index event in patients with coronary heart disease and evidence-based secondary preventive medication. Method: All patients had acute coronary angiography, 679 were discharged from hospital receiving usual care (Hosp), 795 completed a comprehensive Rehab. Follow-up was 12 months. Results: Rehab patients were older (64 vs. 62 years; p < 0.001), had more multivessel disease (51 vs. 37%; p < 0.001), heart failure (64 vs. 40%, p < 0.001), ST-segment elevation myocardial infarction (59 vs. 52%, p = 0.014), and renal insufficiency (10 vs. 7%, p = 0.036). Gender, peripheral artery disease, diabetes, hypertension, and socioeconomic status were similar in groups. Rehab patients had more beta-blockers (88 vs. 75%, p < 0.001) and angiotensin-converting enzyme inhibitors (81 vs. 70%, p < 0.001), a lower low-density lipoprotein cholesterol (102 vs. 122 mg/dl, p < 0.001), and a higher proportion of non-smokers (44 vs. 39%, p = 0.024). Primary combined endpoint of mortality, myocardial infarction (MI), revascularization, and hospitalization occurred in 32.6% of Rehab patients and in 38.7% of Hosp patients [p = 0.014; absolute risk reduction 0.0615, relative risk reduction 16%, number needed to treat (NNT) 17]. Myocardial infarction (MI) (1.8 vs. 3.8%, p = 0.015; NNT 49) and hospitalization (31.8 vs. 38.0%, p = 0.013; NNT 17) were reduced. In multivariate analysis, primary endpoint was reduced significantly (OR 0.729; 95% CI 0.585–0.909; p = 0.005) giving a relative risk reduction of 27% in favour of Rehab. Conclusion: Although Rehab patients were sicker at entry, their outcome was substantially improved within 12 months. With very low NNT, Rehab is highly effective and should be advised to all suitable patients with coronary heart disease.

Cardiac release and kinetics of endothelin after severe short-lasting myocardial ischemia

OBJECTIVES The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia. BACKGROUND Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated. METHODS A coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia. RESULTS In the study group, pacing stress induced severe ischemia (mean duration +/- SD 6.1 +/- 1.2 min), with a maximum of 0.34 +/- 0.12-mV ST segment depression in 21 of 23 patients and angina pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 +/- 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients a transient elevation of Mb with a maximum after 3 h was detected (86.4 +/- 27.1 micrograms/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 +/- 0.8 [baseline] to 12.9 +/- 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 +/- 0.7 [baseline] to 8.3 +/- 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In a control group of 18 patients without heart disease, all variables were unchanged. CONCLUSIONS Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.

Cardiac Release and Kinetics of Endothelin After Uncomplicated Percutaneous Transluminal Coronary Angioplasty

This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 +/- 2.6 pg/ml (mean +/- SD) in the coronary sinus and 7.9 +/- 2.2 pg/ml (mean +/- SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistent cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.

Validation of 12-lead tele-electrocardiogram transmission in the real-life scenario of acute coronary syndrome

A 12-lead electrocardiogram (ECG) recorded in patients with acute coronary syndrome (ACS) was transmitted to a call centre via telephone (tele-ECG). In 120 patients (mean age 64 years) referred to hospitals because of ACS, a standard 12-lead ECG and a tele-ECG recorded at the same time were compared by two cardiologists and one internist independently and blindly. Conduction times exhibited very good agreement between standard and tele-ECG with reliability coefficients (R) of 0.91, 0.86 and 0.89 for the PQ-, QRS- and QT interval, respectively. Rhythm analysis was correct in 99% of the cases. Negative T waves, ST-segment elevation and depression were detected with very high agreement in the tele-ECG exhibiting kappa (κ) coefficients between 0.75 and 0.96. The correct ECG diagnosis of ST-elevation myocardial infarction (STEMI) was possible with excellent agreement between standard and tele-ECG, showing κ coefficients of 0.96, 0.99 and 0.99, respectively, for three investigators. The 12-lead tele-ECG recorder proved accurate for the detection of acute STEMI.

The TeleGuard trial of additional telemedicine care in CAD patients. 2 Morbidity and mortality after 12 months

Summary In the TeleGuard trial, 1500 patients with established coronary artery disease (CAD) were recruited and randomized to control or intervention groups. Patients in the intervention group were equipped with a 12-lead event recorder and could contact a call centre and transmit an ECG whenever they wished. In a 12-month study, the composite endpoint (all-cause mortality, myocardial infarction, re-hospitalization or re-vascularization) was seen in 40% of the intervention patients and in 38% of the control patients. In both groups, approximately 40% were re-hospitalized. In total, 73 patients experienced re-vascularization, 75 showed an infarction and 33 died. Equipping CAD patients with a 12-lead ECG device and providing a telemedicine centre with 24-hour availability did not decrease risk for the composite endpoint (re-hospitalization, re-vascularization, (subsequent) myocardial infarction and/or death). It is likely that the clinical pathway used in the telemedicine centre led to an increased hospital admission rate in the intervention group.