Cihangir Kaymaz

Intravenous thrombolytic treatment of mechanical prosthetic valve thrombosis: a study using serial transesophageal echocardiography.

OBJECTIVE We analyzed the results of intravenous thrombolytic treatment under transesophageal echocardiographic (TEE) guidance in prosthetic valve thrombosis. BACKGROUND Thrombotic occlusion of prosthetic valves continues to be an uncommon but serious complication. Intravenous thrombolytic treatment has been proposed as an alternative to surgical intervention. METHODS In a four-year period, 32 symptomatic patients with prosthetic valve related thrombosis underwent 54 thrombolytic treatment sessions for the treatment of 36 distinct episodes. All patients had low international normalized ratio values at the presentation. Transesophageal echocardiography was performed at baseline and repeated after each thrombolytic treatment session (total 98 TEE examinations). Streptokinase was used as the initial agent with a repeat dose given within 24 h when necessary. Recurrent thrombosis was treated either with tissue plasminogen activator or urokinase. RESULTS The initial success after first dose was only 53% (17/32) but increased up to 88% (28/32) after repeated thrombolytic sessions upon documentation of suboptimal results on TEE examination (p < 0.01). In addition, four asymptomatic patients with large thrombi were also successfully treated with single infusion. The TEE characteristics of thrombus correlated with clinical presentation and response to lytics. Success was achieved with single lytic infusion in 40% of the obstructive thrombi as compared with 75% of the nonobstructive ones (p < 0.05). The success rates of lytic treatment were similar for mitral versus aortic valves, and for tilting disk versus bileaflet valves. Rapid (3 h) and slow (15 to 24 h) infusion of streptokinase resulted in similar success rates. However, major complications (three patients) occurred only in the rapid infusion group. CONCLUSION In patients with prosthetic valve thrombosis, intravenous slow infusion thrombolysis given in discrete, successive sessions guided by serial TEE and transthoracic echocardiography can be achieved with a low risk of complications and a high rate of success.

Acute effect of cigarette smoking on heart rate variability

Acute cigarette smoking enhances adrenergic activity and thus may be associated with hemodynamic changes in the cardiovascular system. In this study, the acute effect of cigarette smoking on heart rate variability (HRV) was studied. Fifteen subjects were included in the study. Time domain (the mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences) and frequency domain (high-frequency, low-frequency ratio, and low-frequency/high-frequency ratio) parameters of HRV were obtained from all participants for each 5-minute segment: 5 minutes before and 5, 10, 15, 20, 25, and 30 minutes after smoking a cigarette. The mean R-R interval, the standard deviation of R-R interval, and the root mean square of successive R-R interval differences significantly decreased within the first 5-minute period compared with baseline, and then the standard deviation of R-R interval increased within the 20- to 30-minute period. The low-frequency high-frequency ratio significantly decreased within the first 5 minutes after smoking and then remained unchanged throughout the study period. Similarly, low-frequency and high-frequency power increased within the first 5 minutes compared with baseline. Acute cigarette smoking alters HRV parameters, particularly within the first 5 to 10 minutes after smoking.

Increased right ventricular glucose metabolism in patients with pulmonary arterial hypertension.

Background and Aims: We aimed to assess the characteristics of glucose utilization in left and right ventricle (LV, RV) myocardium with F-18 fluorodeoxyglucose (FDG) on positron emission tomography in patients with pulmonary arterial hypertension (PAH), and to evaluate whether predominance of RV glucose metabolism as compared with that in LV relates to clinical, hemodynamic, echocardiographic, and neurohormonal parameters. Methods: The study group comprised 23 patients with PAH and 16 healthy controls who underwent FDG positron emission tomography. The ratio of RV uptake (u) of FDG to those of LV was used as a marker for the glucose utilization by RV myocardium. Six-minute walking distance, plasma brain natriuretic peptide (BNP), planimetric echo measures of RV and LV areas, pulmonary arterial systolic pressure estimated by Doppler, Tei index, tricuspid annular excursion, and systolic tissue velocity (St) were used to assess the RV function. Results: The patients with PAH had significantly higher FDG SUV ratios as compared with controls. The RV to LV FDGu ratio showed a high correlation with PAPs (r = 0.87, P < 0.05), BNP (r = 0.63, P < 0.05), and planimetric echo measures of RV to LV area ratio (r = 0.61, P < 0.05); a mild correlation with Tei index (r = 0.47, P < 0.05); and a high and inverse correlation with tricuspid annular excursion (r = −0.80, P < 0.05), 6-minute walking distance (r = −0.74, P < 0.05), and St (r = −0.68, P < 0.05). Conclusions: Increased RV myocardium FDG accumulation indicates increased RV loading that correlates with prognostic markers in pulmonary hypertension including reduced exercise capacity, elevated BNP, and echo variables of tricuspid annular function. Moreover, identification of increased RV FDG accumulation predicts the presence but not the severity of elevated pulmonary systolic pressure.

The risk of false results in the assessment of platelet function in the absence of antiplatelet medication: Comparision of the PFA-100, multiplate electrical impedance aggregometry and verify now assays

OBJECTIVES Evaluation of aspirin (ASA) responsiveness with platelet function tests varies by the choice of blood mixture and functional test and cut off values for defining the the treatment used. Addition to that we also aimed to determine agreement between three tests and to research whether there is any necessity to measure baseline platelet activity. METHODS The study group comprised of 52 patients with multiple risk factors receiving primary prophylaxis of ASA (100 mg/day). For each patient inhibition of platelet aggregation with aspirin was determined using three different whole blood tests: Multiplate electrical impedance aggregometry, Verify Now Aspirin, and collagen-epinephrine closure time PFA-100. Platelet aggregation was assessed with multiplate electrical impedance aggregometry,and was defined as the area under curve (AUC,AUxmin). Maximal 6,4 microM collagen-induced AUC were used to quantify platelet aggregation due to ASA. The ASA response was defined as >30 % reduction in basal platelet aggregation with multiplate electrical impedance aggregometry. Collagen induced platelet aggregation at the Verify Now Aspirin assay quantitated the ASA-induced platelet inhibition as aspirin reaction units (ARU). According to manufacturer insert ARU>550 indicates aspirin resistance. ASA platelet function studies were assessed twice at baseline (pre-aspirin), and after 7 day(post-aspirin) were performed. RESULTS After ASA intake none of the patients was found aspirin resistant with PFA-100. (CEPI-CT (129+/-36 vs 289+/-18 ). None of the patients was found aspirin resistant with PFA-100. As>30 % reduction in basal platelet aggregation with multiplate electrical impedance aggregometry is selected all of the patients have been stratified as responders.(COL TEST 688+/-230 vs 169+/-131 AU) None of the patients with Verify Now Aspirin found resistance to ASA(594+/-62 vs 446+/-43).Prior to ASA intake 15 of all patients with VN(501+/-16) and 2 of all patients with multiplate electrical impedance aggregometry (223+/-40 AUC )aggregation levels below the cut off label before ingestion of ASA.None of the patients was above the cut off label with PFA -100 (129+/-36). CONCLUSIONS Verify Now ASA assay, multiplate electrical impedance aggregometry and PFA-100 seem to be reliable tests in reflecting ASA effect on platelets. Cut off labels for the defining the responsiveness given by manufacturer may show significant interindividual variability with Verify Now ASA assay and multiplate electrical impedance aggregometry, and these test may show platelet inhibition despite the absence of ASA intake. Consideration of the pretreatment values may eliminate the risk of overestimation in the assessment of platelet inhibition by ASA.

Enhanced hemostatic indices in patients with pulmonary arterial hypertension: An observational study

BACKGROUND Pulmonary arterial hypertension (PAH) is a chronic progressive disease characterized by persistent elevation of pulmonary artery pressure. Regardless of the initial trigger, the elevated pulmonary arterial pressure and vascular resistance in patients with PAH are primarily caused by remodeling and thrombosis of small- and medium-sized pulmonary arteries and arterioles, as well as sustained vasoconstriction. Recent studies have emphasized the relevance of several biomarkers of hemostasis in the PAH progression. However, there is no agreement whether hemostatic indices are indeed distinguishing PAH patients from controls. METHODS Plasma fibrinogen, D-dimer, platelet count, and mean platelet volume, and platelet aggregation induced by ADP and collagen were serially measured in 34 patients with PAH, and 34 matched by age and sex normal volunteers. RESULTS Hemostatic indices were significantly higher for fibrinogen (p=0.0001), D-dimer (p=0.001), mean platelet volume (p=0.001), and platelet aggregation induced by ADP-, and collagen (p=0.0001 for both) in PAH patients when compared to healthy controls. In contrast, platelet counts were almost identical between both groups. CONCLUSIONS Patients with PAH exhibit activation of hemostatic indices compared to healthy controls. These data support previous observations that hemostatic abnormalities including platelet activation may directly impact pathogenesis of PAH, and need to be confirmed in larger randomized studies with more comprehensive assessment of hemostatic indices for justification of antithrombotic strategies.

Cardiac Hydatid Cysts

Abstract  From 1991 to 2000 six patients with intracardiac echinococcosis underwent surgical treatment. Four patients were females and two were males, age of the patients ranged from 20 to 68 years. Two patients had symptoms, all patients were diagnosed as a component of multi‐organ echinococcosis and three of them underwent operation before. They were examined serologically and echocardiographically. Cardiac hydatidosis were diagnosed in right ventricle (in three cases), left ventricle (in one case), and interventricular septum (in two cases). Sternotomy was the approach used and all patients were operated on using cardiopulmonary bypass. Intraoperative rupture did not occur. There was no operative mortality, the only morbidity was complete atrioventricular block necessitating VVD pacemaker implantation in the patient with hydatid cyst involving the basal interventricular septum. All patients were followed by medical treatment with albendazole (400 mg/day) and no recurrences were reported in the late follow‐up.

Kounis syndrome presenting with cardiogenic shock

Kounis syndrome has been found to be associated with coronary artery spasm and acute coronary syndrome developing due to mast cell degranulation. It is relatively newly described and is being reported more and more frequently. The drugs, endovascular devices, environmental agents and several allergic diseases likely to cause Kounis syndrome have been described. All patients presented with acute coronary syndrome and anaphylactic shock in the absence of hemodynamic failure. No patient was reported with cardiogenic shock.

Assessment of Left Ventricular Functions in Patients With Isolated Coronary Artery Ectasia by Conventional and Tissue Doppler Imaging

The authors sought to determine left ventricular functions by conventional and tissue Doppler imaging in patients with isolated coronary artery ectasia and controls. Peak early (E) and late (A) mitral inflow velocity, E/A ratio, E deceleration time, and isovolumetric relaxation time were obtained. Peak systolic velocity (Sm), diastolic early (Em), and late (Am) velocities were measured by tissue Doppler imaging. Interventricular septum velocities, including peak systolic (Ss), diastolic early (Es), and late (As) velocities, were recorded. Peak early (E) velocity, E/A ratio, and E deceleration time were different in both groups. Isovolumetric relaxation time was prolonged in patients with coronary artery ectasia than controls. Em and Em/Am ratio were lower in patients with coronary artery ectasia than controls. Diastolic early and Es/As velocities were lower in patients with coronary artery ectasia compared with controls. The authors showed that mitral inflow-lateral annulus and interventricular septum velocities were lower in patients with coronary artery ectasia than controls indicating left ventricular diastolic dysfunction.

Identifying Cardiovascular Risk Factors in a Patient Population With Coronary Artery Ectasia

Coronary artery ectasia (CAE) is frequently considered as a form of coronary artery disease. Cardiovascular risk factors were determined in a patient population with CAE. The 51 patients with isolated CAE (group 1), 61 patients with CAE coexisting with significant coronary stenosis (group 2), and 62 subjects with significant coronary stenosis (group 3) were included in the study, and the distribution of cardiovascular risk factors was compared. Thirty of 51 patients with isolated CAE had presented with typical angina pectoris, 8 patients with unstable angina pectoris, and 13 patients had atypical chest pain or palpitation. The 21 of 51 patients with isolated CAE had definitive positive treadmill exercise test results. Positive family history was similar in each group. The history of smoking was similar in group 1 and group 2 but higher than group 3. Frequency of hypertension was similar in group 1 and group 2 but higher than that in group 3. Frequency of diabetes mellitus was similar in group 1 and group 2 but lower than group 3. Plasma lipid levels and the number of patients with lipid disturbances were also similar in each group. In addition, C-reactive protein (CRP) levels were above the normal limits and there was no difference among groups with respect to plasma CRP levels. CAE appears to be associated with traditional cardiovascular risk factors such as hypertension, smoking, and hyperlipidemia. In addition, elevated CRP level in patients with CAE may suggest the role of inflammatory process in development of CAE.

The Risk of Atrial Fibrillation With Ivabradine Treatment: A Meta-analysis With Trial Sequential Analysis of More Than 40000 Patients.

Recent trials reported that risk of atrial fibrillation (AF) is increased in patients using ivabradine compared with controls. We performed this meta‐analysis to investigate the risk of AF association with ivabradine treatment on the basis of data obtained from randomized controlled trials (RCTs). We searched PubMed, EMBASE, Scopus, and the Cochrane Library for RCTs that comprised >100 patients. The incidence of AF was assessed. We obtained data from European Medicines Agency (EMA) scientific reports for the RCTs in which the incidence of AF was not reported. We used trial sequential analysis (TSA) to provide information on when we had reached firm evidence of new AF based on a 15% relative risk increase (RRI) in ivabradine treatment. Three RCTs and 1 EMA overall oral safety set (OOSS) pooled analysis (included 5 RCTs) were included in the meta‐analysis (N = 40 437). The incidence of AF was 5.34% in patients using ivabradine and 4.56% in placebo. There was significantly higher incidence of AF (24% RRI) in the ivabradine group when compared with placebo before (RR: 1.24, 95% confidence interval: 1.08‐1.42, P = 0.003, I 1980 = 53%) and after excluding OOSS (RR: 1.24, 95% confidence interval: 1.06‐1.44, P = 0.008). In the TSA, the cumulative z‐curve crossed both the traditional boundary (P = 0.05) and the trial sequential monitoring boundary, indicating firm evidence for ≥15% increase in ivabradine treatment when compared with placebo. Study results indicate that AF is more common in the ivabradine group (24% RRI) than in controls.