Abstract Aim We aimed to determine the predictors of early death in the course of acute pulmonary embolism (APE). Materials and methods We included 206 patients who had been admitted to our hospital ...between January 2011 and April 2013 with the diagnosis of APE. We derived a new model including corrected QT interval dispersion (QTcd) and P wave dispersion (Pd), echocardiographic findings, laboratory markers, and blood cell count indices to predict early death in patients with APE. Results Thirty patients (14.5%) died; 176 patients (85.5%) lived after diagnosis of APE. Logistic regression (LR) analysis found that troponin I (odds ratio OR, 1.084 95% confidence interval {CI}, 1.009-1.165), creatinine (OR, 4.153 95% CI, 1.375-12.541), mean platelet volume (OR, 1.991 95% CI, 1.230-3.223), neutrophil to lymphocyte ratio (NLR) (OR, 1.079 95% CI, 1.005-1.160), QTcd (OR, 1.084 95% CI, 1.043-1.127), Pd (OR, 1.049 95% CI, 1.004-1.096) were associated with early death in APE. New LR model (area under the curve AUC, 0.970) performed better than the simplified pulmonary embolism severity index (sPESI) score (AUC, 0.859) in predicting early death in APE ( P = .021). The predictivity of the sPESI score significantly improved after its single combination with creatinine, QTcd, or troponin I. When the combined model was constructed together with these 6 independent variables and sPESI score, stepwise LR model automatically excluded Pd and NLR, and the AUC from the rest of the combined model was 0.976, which is significantly different from the AUC of sPESI (0.859) ( P = .0031). Conclusions Creatinine, troponin I, and QTcd significantly improves sPESI score. A new model with troponin I, creatinine, mean platelet volume, NLR, QTcd, and Pd seems to have greater prognostic power than the sPESI scoring system.
Objective: This study investigated the cardiotoxicity of cisplatin (CIS) on rat heart
by using the oxidative damage of the rat myocardium, troponin I and serum S100A1
levels. Previous studies have ...reported that cell-protective effect of Pycnogenol®
(PYC) depended on its antioxidant and anti-inflammatory properties. Hence, the
myocardial protective effect of PYC was investigated in this study.
Materials and Methods: Rats were randomly grouped to four with 5 rats in each
group. The groups were consisted of control group, PYC group: 10 mg/kg PYC for 7
days, CIS group: 15 mg/kg single injection of CIS on the 5th day, CIS + PYC group:
10 mg/kg PYC for 7 days, plus 15 mg/kg single injection of CIS on the 5th day. Heart
and serum samples were acquired subsequently.
Results: CIS and PYC co-treatment group had increased catalase level (from
43.61±15.16 to 60.80±21.36, p<0.019) and prevented troponin I elevation (from
7.34±6.20 to 3.03±1.36). The S100A1 level was significantly reduced by CIS (from
10.25±8.8 to 3.99±2.87, p<0.035) and was restored by PYC treatment (32.07±29.23).
Conclusion: Injured cardiomyocytes released troponin I after exposure to CIS
and PYC, which can protect the cells from CIS cardiotoxicity, increased the tissue
catalase level. Additionally, PYC treatment increased serum level of S100A1.
IntroductionCoronary artery ectasia (CAE) is localized or diffuse enlargement of the coronary artery more than 1.5 times in diameter in comparison with the adjacent normal coronary artery. The ...etiology and pathophysiology of CAE are not fully elucidated. Resistin is a newly identified adipocyte secreted hormone belonging to a cysteine-rich protein family. Recently it has been found to be relevant to inflammation-related disease and correlated with serum C-reactive protein (CRP). This research aimed to investigate whether the resistin level has a role in CAE etiopathogenesis. Material and methodsA hundred and three patients with diagnosis of CAE and 122 with normal coronary anatomy (NCA) were included. Details of baseline clinical characteristics and angiographic findings were recorded. Other necessary biochemical parameters were measured with an autoanalyzer. Blood was collected and stored for serum resistin level analysis. ResultsSerum resistin levels in CAE were higher than in the NCA group and were statistically significant (p = 0.001). Hypertension (OR = 1.006, 95% CI: 1.002-1.008, p = 0.025), tobacco use (OR = 1.089, 95% CI: 1.055-1.124, p < 0.001), serum resistin levels (OR = 2.431, 95% CI: 1.100-4.696, p = 0.01), hyperlipidemia (OR = 1.005, 95% CI: 1.000-1.014, p = 0.004), triglyceride (OR = 1.006, 95% CI: 1.001-1.010, p = 0.012) remained as independent factors for CAE. In the subgroup analysis of the CAE group, in patients with ectasia in three coronary arteries, resistin levels were significantly higher and statistically significant (p = 0.001). In ROC analysis, the sensitivity of serum resistin was 67.6% and specificity was 86.7% (AUC = 0.749, 95% CI: 0.621-0.877, p = 0.0001). ConclusionsSerum resistin level was significantly higher in CAE. In addition this study showed that serum resistin levels are directly proportional to the number of coronary arteries with ectasia. We think that this study will shed light on this subject and encourage further studies in this field.
Introduction
Coronary artery ectasia (CAE) is localized or diffuse enlargement of the coronary artery more than 1.5 times in diameter in comparison with the adjacent normal coronary artery. The ...etiology and pathophysiology of CAE are not fully elucidated. Resistin is a newly identified adipocyte secreted hormone belonging to a cysteine-rich protein family. Recently it has been found to be relevant to inflammation-related disease and correlated with serum C-reactive protein (CRP). This research aimed to investigate whether the resistin level has a role in CAE etiopathogenesis.
Material and methods
A hundred and three patients with diagnosis of CAE and 122 with normal coronary anatomy (NCA) were included. Details of baseline clinical characteristics and angiographic findings were recorded. Other necessary biochemical parameters were measured with an autoanalyzer. Blood was collected and stored for serum resistin level analysis.
Results
Serum resistin levels in CAE were higher than in the NCA group and were statistically significant (p = 0.001). Hypertension (OR = 1.006, 95% CI: 1.002–1.008, p = 0.025), tobacco use (OR = 1.089, 95% CI: 1.055–1.124, p < 0.001), serum resistin levels (OR = 2.431, 95% CI: 1.100–4.696, p = 0.01), hyperlipidemia (OR = 1.005, 95% CI: 1.000–1.014, p = 0.004), triglyceride (OR = 1.006, 95% CI: 1.001–1.010, p = 0.012) remained as independent factors for CAE. In the subgroup analysis of the CAE group, in patients with ectasia in three coronary arteries, resistin levels were significantly higher and statistically significant (p = 0.001). In ROC analysis, the sensitivity of serum resistin was 67.6% and specificity was 86.7% (AUC = 0.749, 95% CI: 0.621–0.877, p = 0.0001).
Conclusions
Serum resistin level was significantly higher in CAE. In addition this study showed that serum resistin levels are directly proportional to the number of coronary arteries with ectasia. We think that this study will shed light on this subject and encourage further studies in this field.
A 41-year-old female was admitted to our hospital with an unidentified source of fever, dyspnea and dizziness. Transthoracic echocardiography demonstrated severe mitral valve regurgitation, and ...further examination with transesophageal echocardiography (TEE) revealed a 7 mm vegetation on the anterior mitral leaflet. Blood cultures were negative, and after 45 days of empiric 12 g/day ampicillin-sulbactam therapy, the vegetation was shown to have disappeared. However, due to ongoing severe mitral regurgitation and valve deformity, a prosthetic metallic mitral valve replacement was performed. After the operation, TEE was performed again due to subfebrile fever; however, the valve was normal and blood cultures were negative. Because of the probable relapse risk of infective endocarditis, the preoperative intravenous antibiotherapy was continued for 21 days and then orally for one week. Then, she was placed on follow-up by our outpatient clinic. As her INR was highly unstable during this period and she developed new-onset subfebrile fever, she was hospitalized again, and the TEE demonstrated vegetation. Blood cultures were still negative, and a combination of vancomycin-rifampicin-gentamicin was started. While under that therapy, first stroke and after a few days recurrent trans-ischemic attack developed, and the vegetation was seen to have enlarged. Urgent valve operation was performed with a bioprosthetic mitral valve, and ampicillin-sulbactam therapy was added to her previous antibiotherapy at the suggestion of the Microbiology Department. Oral anticoagulant therapy was planned for three months; however, during the postoperative period, her INR levels were highly unstable and could not be maintained in therapeutic ranges for even two consecutive days. Adjusted dosage of dabigatran to 110 mg/bid according to renal clearance in combination with 150 mg/day aspirin was started. However, valve thrombosis and a massive stroke developed under this therapy. The thrombosis disappeared after continuous heparin infusion, and she was discharged with neurological sequelae on 150 mg/day aspirin 55 days after her last operation. During the follow-up period of four months, no other clinical events occurred.
We report a 57-year-old patient with acute anterior wall infarction with a history of a coronary baypass graft operation in 2007. He also had concurrent left arm cyanosis and severe pain. He had ...received diagnosis of pancreatic adenocarcinoma one month previously and had had his first chemotherapy in the previous week with gemcitabine and 5-fluorouracil. After the angiography, a giant thrombus was detected in the proximal left subclavian artery, deteriorating the flows of both left internal mammarian artery (LIMA) to left anterior descending (LAD) coronary artery graft, as well as the left brachial artery. The proximal subclavian artery was stented and good flow was achieved. Through the LIMA, the distal part of LAD, which was totally obstructed with probable distal thrombus embolization, was reached and a percutaneous balloon angioplasty performed. However, the no-reflow phenomenon was observed in distal LAD. A Fogarty traction of thrombus was performed successfully for the revascularization of the left arm. Approximately 30 minutes after the procedure, both angina and ST segment elevation in ECG were resolved under unfractioned heparin and nitroglycerin infusion. However, the patient died due to sepsis seven days after admission to hospital. In the literature, there are only a few previous reports on this rare clinical entity. The eitology, presentation, and the possible management strategies of this clinical entity is presented in this report.
The increasing frequency of cardiac device use has led to an increase in complication rates. The standard treatment for cardiac device-related infections is removal of the entire pacemaker system and ...reimplantation from the contralateral side after systemic antibiotherapy. The efficacy of various conservative treatments has been established for many years, but there is conflicting information in the literature regarding long-term efficacy.
Our study investigated the long-term efficacy of conservative treatment in patients with pacemaker pocket site infection.
In this retrospective study, according to the exclusion criteria, 132 patients were included. Patients were divided into conservative and standard treatment groups. Conservative treatment was considered to be opening the pacemaker pocket capsule, removing all infected and necrotic tissue, cleaning the capsule, and embedding the battery in the prepectoral region in the subpectoral muscle region.
The follow-up time was 36 ±12.96 months in the conservative treatment group and 39.6 ±10.8 months in the standard treatment group. During this period, no re-infection at the pacemaker pocket site was observed in either group. Examination of the swab cultures of the patients' pacemaker wounds revealed negative culture results in 15 patients (15 out of 60) in the conservative treatment group. In the standard treatment group, 60 patients (60 out of 72) were culture-negative. This difference was statistically significant (
= 0.04).
After a rigorous evaluation, conservative treatment is considered effective and safe in the long term in patients with device pocket site infection.
A 23-year-old male who had a VDDR pacemaker implanted seven years ago due to sick sinus syndrome and recurrent syncope episodes was admitted with symptoms of dyspnea, fever, and tachycardia, which ...were present for a few days. He was suspected to be suffering from pneumonia and underwent computed tomography scanning of the thorax, which revealed widespread infiltration in the lung parenchyma and pulmonary emboli. Transthoracic echocardiography revealed an extremely mobile echogenic structure in the right atrium, which was determined to be the free portion of a ruptured pacemaker lead. There was an overlying thrombus and/or vegetation-like organized soft tissue within the right ventricle around the lead component. In this article, the rupture of a permanent pacemaker lead, which complicated the course of infective endocarditis associated with pulmonary embolism and pneumonia is reported. We hypothesize that the underlying mechanism for the rupture is soft tissue entrapment within the right ventricle. Unfortunately, this rare and life-threatening situation led to the death of our patient after the surgical removal of the device and its components.
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