Prolonged Tpeak-Tend interval in anti-Ro52 antibody-positive connective tissue diseases.

Patients with connective tissue diseases (CTDs) may have prolonged corrected QT interval which indicates increased risk for ventricular arrhythmias. However, a more sensitive measure of ventricular repolarization, T-peak-to-end (Tpe) interval, has not been studied in CTDs. We aimed to investigate the relationship between ventricular repolarization abnormalities and anti-Ro52-positivity in subjects with connective tissue diseases (CTDs). We enrolled patients with anti-Ro52-positive CTDs, ANA-positive CTDs, and healthy subjects in this cross-sectional study. We excluded conditions potentially affecting the QT interval. We compared the ECG measures between the groups and performed analyses to define factors associated with ventricular repolarization measures. 15 ANA and anti-Ro52-positive, 39 ANA-positive and anti-Ro52-negative, and 22 healthy subjects were enrolled. None of the subjects had rhythm or conduction disturbances. Corrected QT intervals were similar between the groups. Tpe (84, 77.3, and 69.4 msn, respectively) and QT-dispersion (40, 27.2, and 20.1 msn, respectively) were higher in anti-Ro52-positive subjects compared with the ANA-positive and healthy subjects. Anti-Ro52 titers were correlated with Tpe and QT-dispersion (r = 0.52 and p < 0.001 for each). ANA and anti-Ro52-positivity were independently associated with higher Tpe (OR = 7.7, p = 0.001 and OR = 6.9, p = 0.001, respectively), corrected Tpe (OR = 11.3, p = 0.001 and OR = 8.4, p = 0.003, respectively), QT dispersion (OR = 7, p = 0.008 and OR = 13, p < 0.001, respectively), and QTc dispersion (OR = 9.1, p = 0.001 and OR = 14.1, p < 0.001, respectively). This study provides evidence that ANA positivity, especially when concomitant anti-Ro52-positivity is present, significantly deteriorates ventricular repolarization. The aforementioned ventricular repolarization abnormalities may render these subjects susceptible to serious rhythm or conduction disorders in the setting of predisposing conditions.

Catheter-directed ultrasound-accelerated thrombolysis may be life-saving in patients with massive pulmonary embolism after failed systemic thrombolysis.

The treatment options for high risk acute pulmonary embolism (PE) patients with failed systemic thrombolytic treatment (STT) is limited. The clinical use of catheter directed thrombolysis with the EkoSonic Endovascular System (EKOS) in this population has not been evaluated before. Catheter directed thrombolysis is an effective treatment modality for high risk PE patients with failed STT. Thirteen consecutive patients with failed STT were included in the study. EKOS catheters were placed and tissue plasminogen activator (t-PA) in combination with unfractionated heparin were given. Clinical and echocardiographic properties of the patients were collected before EKOS, at the end of EKOS and during the follow-up visit 6 months after discharge. The duration of EKOS treatment was 21.8 ± 3.8 h and the total dose of tPA was 31.2 ± 15.3 mg. One patient who presented with cardiac arrest died and the clinical status of the remaining subjects improved significantly. Any hemorrhagic complication was not observed. EKOS resulted in significant improvement of right ventricular functions and decrease of systolic pulmonary artery pressure. During a follow-up period of 6 months none of the patients died or suffered recurrent PE. In addition, echocardiographic parameters or right ventricular function significantly got better compared to in-hospital measurements. EKOS is an effective treatment modality for high risk PE patients with failed STT and can be applied with very low hemorrhagic complications.

The utility of inferior vena cava diameter and the degree of inspiratory collapse in patients with systolic heart failure.

INTRODUCTION: Both inferior vena cava (IVC) diameter and the degree of inspiratory collapse are used in the estimation of right atrial pressure. AIM: The purpose of this study is to evaluate the utility of IVC diameter, using echocardiography as a marker of volume overload and the relationship between these parameters and N-terminal pro-B natriuretic peptide (NT-proBNP) in patients with systolic heart failure (HF). METHODS: We included 136 consecutive patients with systolic HF (left ventricular ejection fraction, <50%), including 80 patients with acutely decompensated HF and 56 patients with compensated HF as well as 50 subjects without a diagnosis of HF. All patients underwent transthoracic echocardiography to assess both their IVC diameters and the degree of inspiratory collapse (≥50%, <50%, and no change [absence] groups); NT-proBNP levels were measured, and these data were compared between the 2 groups. RESULTS: Inferior vena cava diameter and NT-proBNP were significantly higher among the patients with HF than among the control subjects (21.7 ± 2.6 vs 14.5 ± 1.6 mm, P < .001 and 4789 [330-35000] vs 171 [21-476], P < .001). The mean IVC diameter was higher among the patients with decompensated HF than among the patients with compensated HF (23.2 ± 2.1 vs 19.7 ± 1.9 mm, P < .001). The values of NT-proBNP were associated with different collapsibility of IVC subgroups among HF patients. The NT-proBNP levels were 2760 (330-27336), 5400 (665-27210), and 16806 (1786-35000), regarding the collapsibility of the IVC subgroups: greater than or equal to 50%, less than 50%, and absence groups, P < .001, respectively, among HF patients. There was a significant positive correlation between IVC diameter and NT-proBNP (r = 0.884, P < .001). A cut off value of an IVC diameter greater than or equal to 20.5 mm predicted a diagnosis of compensated HF with a sensitivity of 90% and a specificity of 73%. CONCLUSIONS: Inferior vena cava diameter correlated significantly with NT-proBNP in patients with HF. Inferior vena cava diameter may be a useful variable in determining a patient's volume status in the setting of HF and may also enable clinicians to distinguish patients with decompensated HF from those with compensated HF.

Can infectious endocarditis during pregnancy be cured with only drug treatment?

During pregnancy, infective endocarditis (IE) is quite rare but has a high mortality rate in terms of the mother and the fetus. In this article, a 24-year-old patient with a history of mitral valve prolapse (MVP) who was hospitalized due to IE and treated successfully is presented. On echocardiography, severe mitral valve prolapse, severe mitral regurgitation, and vegetation on the posterior leaflet of mitral valve were observed. Streptococcus mitis was subsequently isolated from four sets of blood cultures. The patient was diagnosed with IE. After 6 weeks of antibiotic therapy, the patient was cured completely without surgical treatment. At 40-weeks of pregnancy, the patient gave birth via a normal vaginal delivery. There were no problems with the 3,800-gram baby born. In current guidelines, there is very limited advice on treatment options for patients who develop IE during pregnancy. Therefore, evaluation of patient-based treatment options would be appropriate. In addition, IE prophylaxis for MVP is not recommended in current guidelines. However, in MVP patients with mitral regurgitation, prior to procedures associated with a high risk of infective endocarditis, IE prophylaxis may be rational.

Diffuse involvement of the heart and great vessels in primary cardiac lymphoma.

Primary cardiac lymphoma (PCL) is an extremely rare disorder. In this report, a 57-year-old male with diffuse large B-cell lymphoma involving the heart and great vessels is presented. Trans-thoracic echocardiography was the first modality used to establish the diagnosis. Fluorine-18-fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) showed diffuse increased metabolic activity of the heart walls and hypermetabolic lesions occupying cardiac chambers in some areas. The patient underwent systemic chemotherapy, and after 13 days, a marked regression of the tumour mass was evident based on echocardiographic examination. After completing six R-CHOP chemotherapy treatments, PET imaging was planned to control the residual mass, but the patient was intubated due to pneumonia that developed after the sixth chemotherapy session and subsequently died due to sepsis.

A rare reason for pulmonary hypertension: primary sarcoma of the pulmonary artery.

Primary sarcoma of the pulmonary artery (PSPA) is an extremely rare tumor of the cardiovascular system. The prognosis is very poor. The clinical symptoms and imaging findings imitate those of pulmonary emboli, causing delays in diagnosis. In this case report, we describe a 73-year-old man with PSPA who initially was admitted with exertional shortness of breath. Transthoracic echocardiographic evaluation revealed 2 masses in the pulmonary artery causing pulmonary hypertension. The patient underwent operation, but he could not be weaned off cardiopulmonary bypass at the end of the operation and died. Pathologic examination of the masses revealed pulmonary sarcoma. Although this patient was admitted to our clinic only 2 weeks after the initial symptoms, he already had distal metastases.

Serum arylesterase activity is negatively correlated with inflammatory markers in patients with acute coronary syndromes.

OBJECTIVES: To examined whether serum paraoxonase (PON1) and arylesterase (ARE) activities are correlated with inflammatory biomarkers (procalcitonin and high sensitivity C-reactive protein (hs-CRP) in patients with acute coronary syndrome (ACS). METHODS: This cross-sectional study was conducted at the Departments of Cardiology and Biochemistry, Uludag University School of Medicine, Bursa, Turkey, from April 2007 to December 2007. Seventy-eight consecutive patients with ACS and 39 healthy controls were investigated. Acute coronary syndrome patients were divided into 3 groups according to their clinical presentation: unstable angina pectoris (UAP) (Braunwald III-B, n=25), non-ST elevation myocardial infarction (NSTEMI) (n=18), and ST-elevation myocardial infarction (STEMI) (n=35). Serum PON1/ARE activities were measured spectrophotometrically. Levels of procalcitonin and hs-CRP were measured by immunoassay. RESULTS: Paraoxonase/ARE activities were significantly lower in all patient groups compared to controls. No correlation between PON1/ARE activities and high-density-cholesterol levels was seen. Among ACS patients, serum ARE activity correlated inversely with baseline and 48-hour procalcitonin (r=-0.577, p=0.009, and r=-0.642, p=0.019) and hs-CRP levels (r=-0.614, p=0.03, and r=-0.719, p=0.044). CONCLUSION: Serum ARE activity is reduced in ACS patients and inversely correlated with inflammatory markers.

Association between paraoxonase 1 activity and severity of coronary artery disease in patients with acute coronary syndromes.

OBJECTIVE: We sought to investigate serum paraoxonase/arylesterase activities in patients with acute coronary syndromes (ACS) and their correlations with the severity and extent of coronary artery disease (CAD). METHODS AND RESULTS: Three groups of patients were investigated: 89 patients with ACS, 54 patients with normal coronary angiograms (no-CAD group), and 27 healthy comparison subjects. ACS patients were divided into three groups according to their clinical presentation: unstable angina pectoris (UAP, Braunwald III-B, n = 31), non-ST elevation myocardial infarction (NSTEMI) (n = 27), and ST-elevation myocardial infarction (STEMI) (n = 31). Serum paraoxonase/arylesterase activities were measured spectrophotometrically. Angiographic CAD extent was expressed both by the number of vessels diseased and by the Gensini scoring system. Results showed that serum paraoxonase/ arylesterase activities and the paraoxonase/high density lipoprotein-cholesterol (HDL-C) ratio were significantly lower in the STEMI, NSTEMI, UAP groups than in no-CAD and control groups. Serum paraoxonase/arylesterase activities and paraoxonase/HDL-C ratio were reduced in patients with 2-vessel disease (VD) and 3-VD compared to the I-VD and no-CAD group (P < 0.001). In patients with ACS, the Gensini score correlated inversely with serum paraoxonase (r = -0.419, P < 0.001), arylesterase (r = -0.492, P < 0.0001), and the paraoxonase/HDL-C ratio (r = -0.377, P < 0.001). Serum arylesterase (r = 0.161, P = 0.03) and paraoxonase (r = 0.135, P = 0.002) activities were positively correlated with HDL-C levels. Serum arylesterase activity (P < 0.0001), gender (P = 0.0037), diabetes mellitus (P = 0.005) and LDL-C levels (P = 0.03) were independent predictors of CAD presence. CONCLUSIONS: Serum paraoxonase/arylesterase activities are reduced in ACS patients and inversely correlated with the severity of CAD.

Procalcitonin in patients with acute coronary syndrome: correlation with high-sensitive C-reactive protein, prognosis and severity of coronary artery disease.

OBJECTIVES: The aim of this study is to determine the relation of high-sensitive serum C-reactive protein (hsCRP) and procalcitonin with presence and severity of coronary artery disease and early prognosis in patients with acute coronary syndrome (ACS). METHODS AND RESULTS: Procalcitonin and hsCRP levels were measured at admission and after 48 hours in 50 patients (41 men, 9 women) with ACS. The patients were assigned to three groups according to their clinical diagnosis: unstable angina pectoris (UAP) (Braunwald III-B), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Incidences of adverse cardiac events were recorded in a 3-month follow-up. Coronary angiography was performed to evaluate presence and severity of coronary artery disease. In the groups of STEMI, NSTEMI and UAP, procalcitonin (P = 0.01 3, P = 0.045 and P = 0.000 1, respectively) and hsCRP (P = 0.000 1, P = 0.01 and P = 0.00 1, respectively) levels were significantly increased. No significant correlation was found between these markers and the presence and severity of coronary artery disease. There was no correlation between procalcitonin and hsCRP levels at admission and after 48 hours and primary end points after 3 months except in the group of UAP with revascularization procedure. In the group of UAP, hsCRP levels at 48 hours were found higher in the patients with a revascularization procedure (P = 0.04). CONCLUSIONS: In conclusion, levels of hsCRP and procalcitonin are increased in patients with ACS but failed to correlate with severity of coronary disease and early prognosis.

Use of tolvaptan in patients hospitalized for worsening chronic heart failure with severe hyponatremia: The initial experience at a single-center in Turkey.

OBJECTIVE: The aim of the present study was to assess the efficacy and safety of tolvaptan for severe hyponatremia (SH) in hypervolemic heart failure (HF) patients within daily clinical practice. METHODS: We restrospectively reviewed our database on tolvaptan as an add-on treatment in hypervolemic patients admitted to our clinic due to deterioration of HF and having hyponatremia resistant to standard therapy. Severe hyponatremia was defined as serum sodium concentration ≤125 mEq/L. The database included demographic, clinical, laboratory, and echocardiographic findings on admission, and numerous outcome measures for oral tolvaptan treatment were used to assess its efficacy and safety. RESULTS: The study group consisted of 56 hypervolemic HF patients with severe hyponatremia (25 female and 31 male) with mean age of 66 years. All patients received a single dose of tolvaptan 15 mg daily for an average of 3.2 days due to severe hyponatremia. Sodium and potassium concentrations, fluid intake, and urine volume increased (p<0.0001, p=0.037, p<0.0001, and p<0.0001, respectively), whereas furosemide dosage, body weight, heart rate, systolic and diastolic blood pressure, and New York Heart Association class decreased significantly in response to tolvaptan treatment, without a rise in serum creatinine or urea concentrations (p<0.0001, p<0.0001, p=0.001, p<0.049, p<0.009 ve p=0.001, respectively). CONCLUSION: In this retrospective, single-centered study conducted in a small group of Turkish patients, short-term treatment with low-dose tolvaptan added to standard therapy of hypervolemic HF patients with severe hyponatremia was well tolerated with a low rate of major side effects and was effective in correcting severe hyponatremia.

Contribution of 99mTc-sestamibi infusion SPECT to the characterization of fixed perfusion defects.

In patients with coronary artery disease, the distinction between scar and viable myocardium by means of myocardial perfusion imaging (MPI) sometimes can be difficult because of the equivocal meaning of fixed perfusion defects. In this study we examined whether addition of a 99mTc-sestamibi infusion study to the standard MPI could provide extra information regarding the fixed defects. Thirty-seven patients underwent standard MPI and an extra SPECT study in which 99mTc-sestamibi was given as a prolonged constant infusion. Of 324 myocardial segments available for analysis, 134 had fixed or resting perfusion abnormalities on standard MPI studies, of which 25% (33/134) in 12 patients showed partial improvement in the perfusion pattern whereas in 6% (8/134) the improvement was very significant in infusion studies. In 19 patients who were also examined with dobutamine echocardiography, 13 showed concordance between echocardiography and infusion MPI. This study suggests that infusion MPI may provide complementary information to the conventional scintigraphy with regard to interpretation of standard myocardial perfusion scans with fixed defects.

Effects of glucose-insulin-potassium solution added to reperfusion treatment in acute myocardial infarction.

OBJECTIVE: Reperfusion treatment modalities used in the routine treatment protocols of acute myocardial infarction (AMI) were found to be ineffective in establishing the nutritional cellular reperfusion in the microvascular environment even they succeed to open the infarct related artery. Glucose-insulin-potassium (GIK) solution, which is presumed to stimulate the glycolytic pathway, is experimentally proven to be the most efficacious substrate for the preservation of energy production and therefore the myocardial viability, in the setting of acute ischemia. METHODS: We compared, 54 patients who suffered AMI and received GIK solution (300 g glucose+50 IU crystallized insulin+80 mEq potassium chloride in one liter solution) in addition to conventional treatment (GIK group) with 27 patients who were traditionally treated (control group) for in-hospital and early-term (1 month) cardiac morbidity. We also compared the two groups in terms of heart rate variability (HRV). RESULTS: Eight patients in the control group developed new-onset symptomatic congestive heart failure whereas only 5 patients in GIK group were found to have such a cardiac morbidity (p=0.01). Reduced HRV (<50 ms) was found in 3 patients of control group whereas no patient in GIK group had abnormal HRV (p=0.01). CONCLUSION: The GIK solution decreased the incidence of new-onset symptomatic congestive heart failure and low HRV after myocardial infarction. Larger multicenter trials need to resolve the questions on the efficiency of metabolic intervention with GIK solution in acute myocardial infarction.

Protective effect of amifostine against toxicity of paclitaxel and carboplatin in non-small cell lung cancer: a single center randomized study.

AIM: In this study we determined the protective role of amifostine against the side effects of the combination of paclitaxel and carboplatin in patients with non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Chemo-naive patients with NSCLC were eligible. Thirty-eight patients were randomized to receive paclitaxel 175 mg/m2 and carboplatin AUC = 6 with amifostine 910 mg/m2 (group B) or chemotherapy alone (group A). The occurrences of hematologic, neurologic, cardiologic toxicities, and ototoxicity were evaluated. RESULTS: All patients completed the six scheduled cycles of therapy. A total of 114 cycles of chemotherapy was given in both groups. Neutropenia grade 3-4 was observed in 11 cycles (9.6%) in group A and 19 cycles (16.6%) in group B (p = 0.16). Paresthesia grade 1 or 2 was observed in 18 of 19 patients of group A and in 8 of 19 patients of group B, following the sixth cycle of chemotherapy (p = 0.018). Two patients of group B and nine patients of group A suffered from sensory motor impairment grade 2 (p = 0.029). There was no clinical evidence in any patient for deterioration in cardiac function. Asymptomatic and transient sinus bradycardia or ventricular premature beats developed in four patients. None of the patients reported vertigo, tinnitus, or hearing loss. CONCLUSION: The addition of the amifostine to the combination of paclitaxel and carboplatin may prevent or reduce the incidence of neurotoxicity in the treatment of NSCLC. Amifostine does not appear to have a preventive role in neutropenia.

Diffuse intra-alveolar haemorrhage as a complication of thrombolytic therapy in acute myocardial infarction.

Diffuse intra-alveolar haemorrhage is a rare complication of thrombolytic therapy (TT). We report a patient who developed haemoptysis due to pulmonary haemorrhage. This diagnosis should be considered in any patients with respiratory distress, diffuse pulmonary infiltrates, and haemoptysis and otherwise unexplained decrease in haemoglobin concentration after thrombolytic therapy.

Usefulness of intravenous metoprolol during positive isoproterenol tilt-table test in the choice of treatment for neurocardiogenic syncope.

BACKGROUND: Isoproterenol tilt-table testing provides a diagnosis of neurocardiogenic syncope in patients with syncope or near-syncope. Although acute beta-blockade may prevent the development of syncope during isoproterenol tilt-table testing, the use of beta-blockers for chronic prophylaxis may not be effective for some patients who show a positive response to isoproterenol tilt-table testing. We evaluated whether the efficacy of intravenous metoprolol in preventing symptoms during repeated tests would be helpful in selecting patients suitable for long-term therapy. METHODS AND RESULTS: We studied 55 patients (35 females, 20 males; mean age 36+/-11 years) who had been chosen from a group referred to our institute with a history of unexplained syncope (> or = 2 syncopal episodes) and a positive response to isoproterenol tilt-table testing. After a positive response to isoproterenol tilt-table testing, 5 mg metoprolol was infused intravenously as a bolus and the test repeated. Thirty-five patients (group 1) showed a positive response again and 20 (group 2) showed a negative response. We started 50 mg metoprolol once a day for patients in group 1 while group 2 was divided into 2 subgroups: the first subgroup (group 2a, 12 patients) was started on 50 mg sertraline or 20 mg paroxetine once a day and the second subgroup (group 2b, 8 patients) was started on 5 mg midodrine orally once a day. Two months later, isoproterenol tilt-table testing was repeated. In group 1, 13 of 35 patients (37%) were positive on isoproterenol tilt-table testing while in group 2, 8 of 20 patients (40%) were positive on isoproterenol tilt-table testing (p not statistically significant). The therapies of the two groups were then interchanged. Two months later (4 months from the beginning of the study), the isoproterenol tilt-table test was repeated. Eleven patients in group 1 (31%) and 6 in group 2 (30%, p not statistically significant) showed a positive response again. CONCLUSIONS: We conclude that acute beta-blockade response to positive isoproterenol tilt-table testing is not a useful predictor for the assessment of chronic prophylaxis for neurocardiogenic syncope.

Lack of association of heart rate variability parameters with head-up tilt-test responses in patients with syncope.

BACKGROUND: Neurocardiogenic syncope is the most common type of syncope. Head-up tilt testing is the investigation of choice for diagnosis of patients with neurocardiogenic syncope. In this study, we aimed to findout any association between heart rate variability parameters and type of tilt-test response in patients with syncope. METHODS AND RESULTS: Forty-nine cases with unexplained syncopal attacks were enrolled into our study and were grouped according to the tilt-test responses. Tilt test was performed in all patients after excluding other causes of syncope. In case of a negative basal tilt-testing, pharmacological tilt testing was performed after 30 min of 5 mg sublingual isosorbide dinitrate. Holter monitoring was done from the beginning of tilt testing upto two hours post-procedure. The heart rate variability parameters analyzed were the mean of all coupling intervals between normal beats, the standard deviation about the mean of all coupling intervals between normal beats, the mean of all 5-min standard deviations of mean of all coupling intervals between normal beats, the proportion of adjacent normal R-R intervals differing by > 50 ms, the root mean square of the difference between successive RRs, and the standard deviation of 5-min mean of all coupling intervals between normal beats and ratio between low and high frequencies. CONCLUSIONS: In 35 patients, the tilt-test was positive, 16 were cardioinhibitor type (Group 1), four cases had a vasodepressor type response (Group 2) and 15 were mixed type (Group 3). Fourteen patients had a negative test result. The heart rate variability measures did not significantly differ among the study groups. The heart rate variability measures were compared between the tilt-test negative (Group 4) and the tilt-test positive groups (Groups 1, 2 and 3) and no statistically significant difference was found.

Serum choline levels in patients with stable angina and acute coronary syndromes: relation to the severity of coronary artery disease.

OBJECTIVE: We sought to investigate whether serum choline levels are increased across the spectrum of coronary artery disease (CAD) manifestations and correlate with the severity of coronary stenosis. METHODS: A total of 36 patients with acute coronary syndrome (ACS) [22 patients with non-ST-segment elevation ACS and 14 patients with ST-segment elevation acute myocardial infarction (STEMI)], 22 patients with stable angina pectoris (SAP), and 18 controls were recruited for the study. In ACS patients, serum choline levels were measured on admission, and at 24 and 48 h thereafter, using high-performance liquid chromatography. The severity of CAD was assessed using the Gensini score. RESULTS: Serum choline levels on admission were significantly higher in the entire group of patients with ACS than in controls. The highest level of choline was observed in the STEMI group, followed by the SAP, and the non-ST-segment elevation ACS groups. Serum choline levels decreased gradually in patients with STEMI over the 48-h period. Serum choline levels on admission, and at 24 or 48 h thereafter, did not correlate with the presence of CAD neither in patients with ACS (P=0.78, 0.98 and 0.98, respectively) nor in those with SAP (P=0.92). CONCLUSION: Our results suggest that serum choline levels are increased in ACS patients. However, there was no clear correlation between levels of choline and the severity and extent of CAD in this patient group.