Evaluation of the relationship between end-tidal carbon dioxide level and heart failure classification.

OBJECTIVE: Heart failure is a disease with cardiac dysfunction, and its morbidity and mortality are associated with the degree of dysfunction. The New York Heart Association classifies the heart failure stages based on the severity of symptoms and physical activity. End-tidal carbon dioxide refers to the level of carbon dioxide that a person exhales with each breath. End-tidal carbon dioxide levels can be used in many clinical conditions such as heart failure, asthma, and chronic obstructive pulmonary disease. The aim of the study was to reveal the relationship between end-tidal carbon dioxide levels and the New York Heart Association classification of heart failure stages. METHODS: This study was conducted at Kahramanmaras Sütçü Imam University Faculty of Medicine Adult Emergency Department between 01/03/2019 and 01/09/2019. A total of 80 patients who presented to the emergency department with a history of heart failure or were diagnosed with heart failure during admission were grouped according to the New York Heart Association classification of heart failure stages. The laboratory parameters, ejection fraction values, and end-tidal carbon dioxide levels of the patients were measured and recorded in the study forms. RESULTS: End-tidal carbon dioxide levels and ejection fraction values were found to be significantly lower in the stage 4 group compared to the other groups. Furthermore, pro-B-type natriuretic peptide (BNP) values were found to be significantly higher in stage 4 group compared to the other groups. CONCLUSION: It was concluded that end-tidal carbon dioxide levels could be used together with pro-BNP and ejection fraction values in determining the severity of heart failure.

Factors of mortality in patients with cardiac implantable electronic device: 5-year experience.

OBJECTIVE: The use of cardiac implantable electronic devices has increased in recent years. It has also brought some issues. Among these, the complications of cardiac implantable electronic devices infection and pocket hematoma are difficult to manage. It can be fatal with the contribution of patient-related risk factors. In this study, we aimed to find mortality rates in patients who developed cardiac implantable electronic devices infection and pocket hematoma over 5 years. We also investigated the risk factors affecting mortality in patients with cardiac implantable electronic devices. METHODS: A total of 288 cardiac implantable electronic devices patients were evaluated. Demographic details, history, and clinical data of all patients were recorded. Cardiac implantable electronic devices infection was defined according to the modified Duke criteria. The national registry was used to ascertain the mortality status of the patients. The patients were divided into two groups (exitus and survival groups). In addition, the pocket hematoma was defined as significant bleeding at the pocket site after cardiac implantable electronic devices placement. RESULTS: The cardiac implantable electronic devices infection was similar in both groups (p=0.919), and the pocket hematoma was higher in the exitus group (p=0.019). The exitus group had higher usage of P2Y12 inhibitors (p≤0.001) and novel oral anticoagulants (p=0.031). The Cox regression analysis, including mortality-related factors, revealed that renal failure is the most significant risk factor for mortality. Renal failure was linked to a 2.78-fold higher risk of death. CONCLUSION: No correlation was observed between cardiac implantable electronic devices infection and mortality, whereas pocket hematoma was associated with mortality. Furthermore, renal failure was the cause of the highest mortality rate in patients with cardiac implantable electronic devices.

Factors of mortality in patients with cardiac implantable electronic device: 5-year experience

SUMMARY OBJECTIVE: The use of cardiac implantable electronic devices has increased in recent years. It has also brought some issues. Among these, the complications of cardiac implantable electronic devices infection and pocket hematoma are difficult to manage. It can be fatal with the contribution of patient-related risk factors. In this study, we aimed to find mortality rates in patients who developed cardiac implantable electronic devices infection and pocket hematoma over 5 years. We also investigated the risk factors affecting mortality in patients with cardiac implantable electronic devices. METHODS: A total of 288 cardiac implantable electronic devices patients were evaluated. Demographic details, history, and clinical data of all patients were recorded. Cardiac implantable electronic devices infection was defined according to the modified Duke criteria. The national registry was used to ascertain the mortality status of the patients. The patients were divided into two groups (exitus and survival groups). In addition, the pocket hematoma was defined as significant bleeding at the pocket site after cardiac implantable electronic devices placement. RESULTS: The cardiac implantable electronic devices infection was similar in both groups (p=0.919), and the pocket hematoma was higher in the exitus group (p=0.019). The exitus group had higher usage of P2Y12 inhibitors (p≤0.001) and novel oral anticoagulants (p=0.031). The Cox regression analysis, including mortality-related factors, revealed that renal failure is the most significant risk factor for mortality. Renal failure was linked to a 2.78-fold higher risk of death. CONCLUSION: No correlation was observed between cardiac implantable electronic devices infection and mortality, whereas pocket hematoma was associated with mortality. Furthermore, renal failure was the cause of the highest mortality rate in patients with cardiac implantable electronic devices.

Evaluation of the relationship between end-tidal carbon dioxide level and heart failure classification

SUMMARY OBJECTIVE: Heart failure is a disease with cardiac dysfunction, and its morbidity and mortality are associated with the degree of dysfunction. The New York Heart Association classifies the heart failure stages based on the severity of symptoms and physical activity. End-tidal carbon dioxide refers to the level of carbon dioxide that a person exhales with each breath. End-tidal carbon dioxide levels can be used in many clinical conditions such as heart failure, asthma, and chronic obstructive pulmonary disease. The aim of the study was to reveal the relationship between end-tidal carbon dioxide levels and the New York Heart Association classification of heart failure stages. METHODS: This study was conducted at Kahramanmaraş Sütçü İmam University Faculty of Medicine Adult Emergency Department between 01/03/2019 and 01/09/2019. A total of 80 patients who presented to the emergency department with a history of heart failure or were diagnosed with heart failure during admission were grouped according to the New York Heart Association classification of heart failure stages. The laboratory parameters, ejection fraction values, and end-tidal carbon dioxide levels of the patients were measured and recorded in the study forms. RESULTS: End-tidal carbon dioxide levels and ejection fraction values were found to be significantly lower in the stage 4 group compared to the other groups. Furthermore, pro-B-type natriuretic peptide (BNP) values were found to be significantly higher in stage 4 group compared to the other groups. CONCLUSION: It was concluded that end-tidal carbon dioxide levels could be used together with pro-BNP and ejection fraction values in determining the severity of heart failure.

Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study.

OBJECTIVE: Severe pulmonary embolism (PE) has a high mortality rate, which can be lowered by thrombolytic therapy (TT). However, full-dose TT is associated with major complications, including life-threatening bleeding. The aim of this study was to explore the efficacy and safety of extended, low-dose administration of tissue plasminogen activator (tPA) on in-hospital mortality and outcomes in massive PE. METHODS: This was a single-center, prospective cohort trial at a tertiary university hospital. A total of 37 consecutive patients with massive PE were included. A peripheral intravenous infusion was used to administer 25 mg of tPA over 6 hours. The primary endpoints were in-hospital mortality, major complications, pulmonary hypertension, and right ventricular dysfunction. The secondary endpoints were 6-month mortality and pulmonary hypertension and right ventricular dysfunction 6 months after the PE. RESULTS: The mean age of the patients was 68.76±14.54 years. The mean pulmonary artery systolic pressure (PASP; 56.51±7.34 mmHg vs. 34.16±2.81 mmHg, P<0.001) and right/left ventricle diameter (1.37±0.12 vs. 0.99±0.12, P<0.001) decreased significantly after TT. Tricuspid annular plane systolic excursion (1.43±0.33 cm vs. 2.07±0.27 cm, P<0.001), myocardial performance index (0.47±0.08 vs. 0.55±0.07, P<0.001), and systolic wave prime (9.6±2.8 vs. 15.3±2.6) increased significantly after TT. No major bleeding or stroke was observed. There was one in-hospital death and two additional deaths within 6 months. No cases of pulmonary hypertension were identified during follow-up. CONCLUSION: The results of this pilot study suggest that an extended infusion of low-dose tPA is a safe and effective therapy in patients with massive PE. This protocol was also effective in decreasing PASP and restoring right ventricular function.

Impact of Sodium-Glucose Cotransporter-2 Inhibitors on Sympathetic Nervous System Activity Detected by Sympathetic Activity Index and LF/HF Ratio in Patients with Type 2 Diabetes Mellitus.

OBJECTIVE: Cardiac autonomic neuropathy is a serious microvascular complication of type 2 diabetes mellitus that affects a significant portion of patients. Due to decreased parasympathetic activity, the sympathetic nervous system becomes dominant, causing several problems that lead to increased cardiovascular morbidity and mortality. Sodium-glucose cotransporter-2 inhibitors have been shown to reduce sympathetic nervous system activity previously. This is a promising finding for restoring the impaired sympathovagal balance in cardiac autonomic neuropathy. The aim of this study is to evaluate the effect of at least 6 months of sodium-glucose cotransporter-2 inhibitor treatment on sympathetic nervous system activity with sympathetic activity index and heart rate variability parameters in patients with type 2 diabetes mellitus. METHODS: Holter-electrocardiogram recordings of 50 patients who were using an sodiumglucose cotransporter-2 inhibitor (empagliflozin or dapagliflozin) for at least 6 months and 50 patients who did not were analyzed retrospectively. The sympathetic activity index and heart rate variability parameters of these 2 groups, which were similar in terms of age, gender, hemoglobin A1c, and duration of diabetes, were compared. RESULTS: The ratio of low-frequency to high-frequency power reflecting the sympathovagal balance [-1.495 (-2.165/-1.196) vs. -1.224 (-1.619/-0.863), P=.008] and sympathetic activity index [1.44 (1.06/2.76) vs. 2.47 (1.42/3.68), P=.009] was lower in the sodiumglucose cotransporter-2 inhibitor group than in the control group. In addition, the sympathetic activity index was correlated with the ratio of low-frequency to high-frequency power (r=0.418, P < .001). CONCLUSION: Sodium-glucose cotransporter-2 inhibitor treatment for at least 6 months was found to result in lower values of sympathetic activity index and the ratio of low-frequency to high-frequency power in patients with type 2 diabetes mellitus. These findings indicate lower sympathetic nervous system activity, which supports the sympathoinhibitor effects of sodiumglucose cotransporter-2 inhibitors.

Dapagliflozin Improves Cardiac Autonomic Function Measures in Type 2 Diabetic Patients with Cardiac Autonomic Neuropathy.

BACKGROUND: Cardiac autonomic neuropathy is a frequent complication of type 2 diabetes mellitus. Cardiac autonomic neuropathy, in which sympathetic tone predominates over parasympathetic activity, increases both cardiovascular morbidity and mortality and unfortunately has no definitive treatment. Sodium-glucose cotransporter-2 inhibitors have been suggested to reduce sympathetic nervous system activity, based on the results from previous studies. In this study, we aimed to investigate the effect of 24-week treatment with dapagliflozin, a sodium-glucose cotransporter-2 inhibitor, on cardiac autonomic function measures in patients with type 2 diabetes mellitus and cardiac autonomic neuropathy. METHODS: Dapagliflozin 10 mg/day (n=42) or non-sodium-glucose cotransporter-2 inhibitor oral antidiabetic(s) (n=38) was added to the treatment of patients whose glycemic control could not be achieved with existing treatments. The patients with definite or confirmed cardiac autonomic neuropathy diagnosed by cardiovascular autonomic reflex tests underwent 24-hour Holter-electrocardiogram recordings to obtain heart rate variability and heart rate turbulence parameters before starting additional medication and after a 24-week treatment period. RESULTS: In-group analyses showed that dapagliflozin 10 mg/day for 24 weeks improved heart rate variability and heart rate turbulence parameters and decreased the frequency of ventricular premature beats relative to their baseline values. No such findings were observed in the control group despite similar glycemic control. Comparisons between dapagliflozin group and the control group showed that these effects of dapagliflozin were significantly better than non-sodium-glucose cotransporter-2 inhibitor oral antidiabetics. CONCLUSION: Dapagliflozin improves measures of cardiac autonomic function compared to the control group in type 2 diabetic patients with cardiac autonomic neuropathy. This intergroup benefit, demonstrated for the first time, may be promising for the regression of cardiac autonomic neuropathy with sodium-glucose cotransporter-2 inhibitors.

Triglyceride glucose index is related with cardiac autonomic dysfunction in patients with metabolic syndrome.

Aim    Cardiac autonomic dysfunction is encountered in approximately 25 % of patients with metabolic syndrome (MetS). 24 hr Holter-ECG based heart rate variability (HRV) and heart rate turbulence (HRT) parameters are used to evaluate cardiac autonomic function. We aimed to investigate the relationship between a novel insulin resistance marker, triglyceride glucose (TyG) index and cardiac autonomic dysfunction in patients with MetS.Material and methods    We examined a total of 400 non-diabetic subjects, 136 with MetS and 264 without MetS. All underwent TyG index calculations, and 24 hr Holter-ECG recordings for the measurement of HRV and HRT parameters.Results    HRV and HRT parameters were lower or higher in patients with MetS than in subjects without MetS, indicating cardiac autonomic dysfunction. We observed significant correlations between TyG index and measures of cardiac autonomic function. Multiple linear regression analysis showed that the TyG index was an independent predictor of almost all HRV and HRT parameters.Conclusion    This study demonstrates the independent relationship between cardiac autonomic dysfunction and the TyG index, a novel marker of insulin resistance in non-diabetic patients with MetS.

Early cardiac electrical and structural changes in patients with non-obese non-alcoholic fatty liver disease.

Background    Obese non-alcoholic fatty liver disease (NAFLD) was found to increase the risk of developing atrial fibrillation (AF) regardless of the metabolic syndrome subgroups that may accompany it. In this study, the effect of NAFLD on the structural and electrical functions of the heart was investigated using tissue Doppler echocardiography (TDE) in non-obese NAFLD patients without any known risk factors for AF.Material and methods    The study included 43 female patients (31.3±3.8 years), who had stage 2-3 hepatosteatosis detected by liver ultrasonography and diagnosed as non-obese NAFLD (patient group), and 31 healthy women (control group, 32.5±3.6 years). In addition to standard echocardiographic parameters, inter- and intra-atrial electromechanical delay (EMD) were evaluated by TDE.Results    Interatrial EMD (PA lateral - PA tricuspid) and intraatrial EMD (PA septum - PA tricuspid) were significantly longer in patient group (16.1±3.4 vs. 12.5±2.3 ms, p<0.001, and 8.4±1.6 vs. 6.6±1.6 ms, p<0.001, respectively). At the subclinical level. atrial size, left ventricular diastolic function, and left ventricular wall thickness measurements were greater in the patient group.Conclusion    Inter-atrial and intra-atrial EMD were detected in young women with non-obese NAFLD. In addition, at the subclinical level, structural and functional impairment was detected However, large-volume prospective studies are required to cobfirm these findings regarding the development of AF in non-obese NAFLD patients.

Evaluation of cardiac functions after catheter ablation of atrioventricular nodal reentrant tachycardia

Background/aim: Radiofrequency catheter ablation (RFA) is the most effective method of supraventricular tachycardia therapy. Recurrent supraventricular tachycardia causes systolic dysfunction and dilated cardiomyopathy. The aim of this study was to evaluate the long-term alterations of atrial and ventricular functions after RFAof typical atrioventricular nodal reentrant tachycardia (AVNRT). Materials and methods: This cross-sectional study included 55 consecutive patients with symptomatic drug-resistant AVNRT who had had an invasive electrophysiology study and RFA. Speckle-tracking­based echocardiographic assessment was performed shortly before and 1 year after the operation. Left ventricle (LV) and right ventricle (RV) peak systolic strain (PSS) and atrial strain measurements were performed. Results: RFA successfully eliminatedtachyarrhythmia in all patients. LV apical 4-chamber PSS ­20.8% (­24.7 to ­16.0) vs. ­22.8% (­26.6 to ­17.0, P < 0.001), LV apical 2-chamber PSS ­21.5% (­26.8 to ­10.1) vs. ­22.0% (­27.8 to ­13.7, P < 0.001), LV global PSS ­20.4% (­26.4 to ­14.4) vs. ­23.0% (­27.1 to ­2.3, P < 0.001), RV global PSS ­26.0% (­30.0 to ­18.0) vs. ­26.5% (­32.1 to ­19.7, P < 0.001), and peak left atrial longitudinal strain 41.0% (19.0­71.8) vs. 54.0% (25.6­82.0, P < 0.001) were significantly improved 1 year after RFA. Conclusion: RFA of AVNRT not only provides relief of palpitations but also improves cardiac functions.

Assessment of cardio-ankle vascular index in patients with abdominal aortic aneurysm: An observational study.

OBJECTIVES: Arterial stiffness is associated with major adverse cardiovascular events. The aim of this study is to investigate arterial stiffness by cardio-ankle vascular index (CAVI) in patients with abdominal aortic aneurysm (AAA). METHODS: This observational and cross-sectional study involved 59 subjects with AAA and 32 healthy subjects. All subjects underwent ultrasonography examination. CAVI was measured by VaSera-1000 CAVI instrument. RESULTS: Mean abdominal aortic diameter of AAA patients and controls were 43.88 ± 9.28 mm and 20.43 ± 3.14 mm, consecutively. Baseline clinical characteristics of the patients and controls were similar for age, presence of hypertension, diabetes, dyslipidemia, coronary artery disease and smoking. Left ventricle ejection fraction and Left ventricle mass index (LVMI) were similar between groups. CAVI was significantly higher in patients with AAA than controls (9.74 ± 1.50 vs. 7.60 ± 1.07, p < 0.001). CAVI was positively correlated with AAA diameter (r = 0.461, p < 0.001) and negatively correlated with left ventricle ejection fraction (r= -0.254, p = 0.015). CAVI >8.3 had a sensitivity 89.8% and a specificity of 78.1% for predicting the presence of AAA in ROC analysis (area under curve = 0.897, 95%CI = 0.816-0.951, p < 0.001). CONCLUSION: CAVI is increased in patients with AAA. Increased arterial stiffness may be a mechanical link between AAA, coronary artery disease and peripheral artery disease or a common mechanism effects the arterial stiffness, coronary artery disease, peripheral artery disease and AAA. Therefore, CAVI may be used as a valuable marker for risk stratification for the development of AAA in susceptible patients.

Clinical safety and efficacy of thrombolytic therapy with low-dose prolonged infusion of tissue type plasminogen activator in patients with intermediate-high risk pulmonary embolism.

: The patients with intermediate-high risk pulmonary embolism who have acute right ventricular (RV) dysfunction and myocardial injury without overt hemodynamic compromise may be candidates for thrombolytic therapy. Alternative low-dose thrombolytic therapy strategies with prolonged infusion may further decrease the complication rates as its efficacy and safety have been previously proven in the management of prosthetic valve thrombosis. In this study, we aimed to investigate the clinical outcomes of low-dose prolonged thrombolytic therapy regimen in intermediate-high risk pulmonary embolism patients. This study enrolled 16 retrospectively evaluated patients (female 9, mean age: 70.9 ±â€Š13.5 years) with the diagnosis of acute pulmonary embolism who were treated with low-dose and slow-infusion of tissue-type plasminogen activator (t-PA). All patients underwent transthoracic echocardiography and computed tomography scan for assessment of thrombolytic therapy success. Low-dose prolonged thrombolytic therapy was successful in all patients. The mean t-PA dose used was 48.4 ±â€Š6.3 mg. There was residual segmental thrombus in nine (56.3%) patients after thrombolytic therapy. The arterial oxygen saturation and tricuspid annular plane systolic excursion increased after thrombolytic therapy whereas heart rate, RV to left ventricular (LV) ratio, systolic pulmonary artery pressure, and the frequencies of hypotension and tachypnea significantly decreased. There was no cerebrovascular accident or major bleeding requiring transfusion. There were two minor bleedings (12.5%) including hemoptysis and epistaxis. Thrombolytic therapy in these intermediate-high risk pulmonary embolism patients was associated with excellent clinical outcomes and survival to discharge (100%) without any 60-day mortality. Prolonged thrombolytic therapy regimen with low-dose and slow-infusion of t-PA may be associated with lower complication rates without comprimising effectiveness in patients with acute intermediate-high risk pulmonary embolism.

The effects of sacubitril/valsartan and ramipril on the male fertility in hypertensive rats.

OBJECTIVE: Renin angiotensinogen system (RAS) inhibitors, ramipril and sacubitril/valsartan are frequently used in the treatment of cardiovascular diseases. Although they are known as contraindicated during pregnancy in hypertensive women, there is not any outcome of their safety in male fertility after exposure to ramipril or sacubitril/valsartan. In this study, we aimed to evaluate the effects of ramipril and sacubitril/valsartan to highlight their safety in the male fertility in normotensive and hypertensive rats. METHODS: Adult male normotensive and dexamethasone-induced hypertensive rats were treated with sacubitril/valsartan, ramipril and saline for 18 days. Arterial blood pressures were verified using carotid artery cannulation. Male fertility parameters, including the testis weights, histopathologic scoring of the testis, sperm count, sperm motility, morphology, and serum testosterone levels, were analyzed in treated and nontreated normotensive/hypertensive rats. RESULTS: Sacubitril/valsartan or ramipril treatments did not reveal a significant difference in sperm production, testicular morphology, and radioimmunoassay of serum testosterone levels compared to the control group. However, sperm motility was significantly reduced in rats under RAS inhibition. CONCLUSION: This finding was likely mediated by the identification of Ang receptors in the tails of rat sperm given that Ang receptors may play a role in the modulation of sperm motility. Identification of RAS-related proteins involved in sperm motility may help to explain their roles in motility. Our data provide general safety evidence for the male fertilization ability after paternal sacubitril/valsartan and ramipril exposure.

Safety of low-dose prolonged infusion of tissue plasminogen activator therapy in patients with thromboembolic events in the intensive care unit.

Objective Thromboembolic events such as acute coronary syndrome related prosthetic heart valve thrombosis, pulmonary artery embolism and renal artery embolism are a rare condition but a major cause of morbidity and mortality. In this study we discussed low-dose thrombolytic therapy, in patients with thromboembolic events in the intensive care unit.Methods The study was performed on 12 consecutive patients [8 female; 50.3±16.0 (35-95) years] with acute thromboembolism including acute coronary syndrome related prosthetic heart valve thrombosis, acute pulmonary embolism and acute renal embolism who were treated with low-dose (25 mg) and slow infusion (6 hours) of t-PA. We evaluated mainly in-hospital safety and also effectiveness.Total treatment episodes was 1.66±0.88 (1-4) times.Results All thromboembolic events have been successfully treated with low-dose (25 mg) and slow infusion (6 hours) of t-PA. The success criteria were clinically improvement and radiologically lysis. None of the patients had ischemic stroke, intracranial hemorrhage, embolism (peripheral and recurrence of coronary artery embolism), bleeding requiring transfusion. The most frequent in-hospital complication was a gum bleeding without need for transfusion (two patients).Conclusions In our case series low-dose (25 mg) and slow infusion (6 hours) of t-PA have been performed successfully for thromboembolic events including acute coronary syndrome related prosthetic heart valve thrombosis, pulmonary embolism and renal embolism in patients with in the intensive care unit. Safety is promising and if efficacy will be proved; this method may be a valuable alternative to standard fibrinolytic regimen.

Management of radio-contrast allergy in radio-contrast allergic patients undergoing coronary angiography and intervention.

Objectives Radiocontrast agents (RCA) allergy occurs in 0.04 % - 0.22 % of patients. However, the risk of allergic reaction increases as 16 % to 35 % in patients with prior RCA allergy. Herein we reported our experience in patients with a prior history of RCA induced anaphylaxis who underwent coronary angiography (CAG) and intervention.Methods This retrospective study included 11 patients with prior history of RCA anaphylaxis who underwent CAG and / or intervention at our clinic between May 2016 and September 2019. The mean age of the patients was 61.8±8.99 years, 8 (72.7 %) were female, 9 (81.8 %) had hypertension, 6 (54.5 %) - diabetes mellitus, 11 (100 %) - dyslipidemia, 8 (72.7 %) patients were current smokers, 4 had prior history RCA allergy after i.v. RCA administration in contrast enhanced computed tomography and 7 patients experienced RCA allergy after CAG. All patients had prior severe anaphylaxis reaction. All patients were pretreated with intravenous feniramin maleat 45.5 mg and methylprednizolone 80 mg one hour before the procedure and dexametazon 8 mg after the procedure.Results CAG and intervention was successfully completed in all patients. Two patients had breakthrough RCA induced anaphylaxis, theyhad urticarial, itching, dyspnea and chest tightness, angioedema during coronary artery stenting. Additional dose of i.v. methylpredinisolene 80 mg, salbutamol nebulae and i.v. adrenalin 1 mg administration rapidly stabilize the patients. All patients were successfully treated and uneventfully discharged after percutaneous coronary intervention.Conclusion Management of patients with prior RCA adverse drug reaction may be complex. However when CAG and / or intervention is required in such patients it may be safely performed with premedication.

Can vasohibin-1, an endothelium-derived angiogenesis inhibitor, be a marker of endothelial dysfunction in hemodialysis patients?

BACKGROUND: Endothelial dysfunction (ED) is associated with high cardiovascular disease burden in hemodialysis (HD) patients. Vasohibin-1, an endothelium-derived angiogenesis inhibitor, is essential for endothelial cell survival, therefore it may be a promising marker of ED. We aimed to investigate whether vasohibin-1 levels are associated with ED markers in HD patients. METHODS: Fifty HD patients and 30 healthy controls were included in the study. As markers of ED, endothelium-dependent flow-mediated dilatation (FMD), carotid intima-media thickness (CIMT), and pulse wave velocity (PWV) were examined. Serum vasohibin-1 levels were measured with ELISA. RESULTS: Serum vasohibin-1 levels were low (387.7 ± 115.7 vs 450.1 ± 140.1 P = .02), FMDs' were impaired (6.65 ± 2.50 vs 10.95 ± 2.86 P < .001), PWV (7.92 ± 1.964 vs 6.79 ± 0.96 P = .01) and CIMT (0.95 ± 0.20 vs 0.60 ± 0.11 P < .001) were increased in HD patients compared to healthy controls. In regression analysis, vasohibin-1 levels were not related with FMD, PWV, or CIMT. CONCLUSIONS: Hemodialysis patients have low serum vasohibin-1 levels but serum levels of vasohibin-1 did not show any significant relationship with FMD, PWV, and CIMT in HD patients. Since vasohibin-1 acts via paracrine pathways, serum levels may be insufficient to explain the relationship between vasohibin and ED. Local vasohibin-1 activity on tissue level may be more important instead of circulating levels.

Association of serum FGF-23, klotho, fetuin-A, osteopontin, osteoprotegerin and hs-CRP levels with coronary artery disease.

Environmental, genetic, oxidative and biochemical factors play an important role in the atherosclerotic process. We investigated the association of serum fibroblast growth factor (FGF-23), klotho, fetuin-A, osteoprotegerin (OPG), osteopontin (OPN) and high-sensitive-CRP (Hs-CRP) markers with coronary artery disease and whether one was superior to others or not. A study group of 52 patients with coronary artery disease (CAD) and a control group of 30 patients with angiographically normal epicardial coronary arteries were included in the study. Serum FGF-23, klotho, fetuin-A, OPN, OPG and Hs-CRP marker levels were studied. Patients with CAD were classified in two groups as low (SYNTAX ≤22, n = 29) and moderate-high (SYNTAX ≥ 23, n = 23) according to anatomic SYNTAX score. FGF-23 (p = .033), klotho (p < .001), fetuin-A (p = .005) and OPG (p = .001) serum marker levels were significantly lower in CAD patients than the control group. Serum levels of FGF-23 (p = .012), klotho (p = .001), fetuin-A (p = .015) and OPG (p = 0.002) were significantly different between SYNTAX tertiles and control group. Klotho (p = .025, odd ratio (OR) = 0.542, 95% confidence interval (CI): 0.317-0.926) and HT (p = .004, OR = 34.598, 95%CI:1.054-1135.657) were the independent predictors of CAD presence. Serum klotho levels of 91.48 pmol/L predicts the presence of CAD with 60% sensitivity and 96.55% specificity (p < .001, area under curve = 0.864, 95% CI = 0.768, 0.931). We found that serum klotho level is an independent predictor of presence, extent and severity of CAD.

Bisoprolol and linagliptin ameliorated electrical and mechanical isometric myocardial contractions in doxorubicin-induced cardiomyopathy in rats.

BACKGROUND: Doxorubicin is an anthracycline chemotherapeutic agent that causes cardiomyopathy as a side effect. Here, we aimed to investigate the effects of linagliptin and bisoprolol on the management of doxorubicin-induced cardiomyopathy in rats. METHODS: Wistar rats were divided into six groups (n = 8). Group I received saline for 4 weeks; group II received 1 mg/kg bisoprolol for 8 weeks; group III received 3 mg/kg linagliptin for 8 weeks; group IV received 1.25 mg/kg doxorubicin for 4 weeks for the induction of cardiomyopathy; group V received 1.25 mg/kg doxorubicin for 4 weeks plus 1 mg/kg bisoprolol for 8 weeks; and group VI received 1.25 mg/kg doxorubicin for 4 weeks plus 3 mg/kg linagliptin for 8 weeks. Electrocardiography and isometric mechanography were conducted to measure ventricular contractile responses. Myocardial tissue and serum samples were analyzed for oxidative and cardiotoxic markers by ELISA. RESULTS: Electrocardiography revealed that QRS, QT and Tp intervals were longer in group IV than group I. Doxorubicin caused a significant decrease in ventricular contraction, which was significantly prevented by bisoprolol. Doxorubicin resulted in myocardial fiber disorganization and disruption, but bisoprolol or linagliptin improved this myocardial damage. Glutathione peroxidase was significantly decreased in groups IV and V. Bisoprolol or linagliptin treatment attenuated the significant doxorubicin-mediated increase in malondialdehyde. Doxorubicin and linagliptin provided significant elevations in CK-MB activity and troponin-I levels. CONCLUSIONS: Doxorubicin resulted in pronounced oxidative stress. The beneficial effects of bisoprolol and linagliptin on myocardial functional, histopathological and biochemical changes could be related to the attenuation of oxidative load.

Endothelial dysfunction predicted increased left atrial volume index in newly diagnosed nondiabetic hypertensive patients.

BACKGROUND: Arterial hypertension is associated with cardiovascular morbidity and mortality. It was previously shown that left atrium volume increase associated with mortality and atherosclerotic heart disease. The aim of the present study was to demonstrate the value of endothelial dysfunction in predicting left atrium volume increase in newly diagnosed hypertension patients. METHODS: This study included 96 consecutive newly diagnosed hypertensive patients. Left atrium volume and left ventricular ejection fraction were calculated. Pulse wave velocity and brachial artery flow-mediated dilation measurements were obtained from each patient. RESULTS: Left Ventricle Mass Index (114 ± 29 g/m, 91 ± 17 g/m, P < 001), left ventricular septum (P < 0.001) and posterior wall thickness (P = 0.001), left ventricular end diastolic diameter (P = 0.016) were significantly higher in patients with higher left atrial volume index. FMD% was lower in patients with higher left atrial volume index those without (9.7 ± 3.5 vs. 13.31 ± 6.01, P = 0.004). Lateral wall E wave velocity was significantly lower (8.68 ± 2.8, 10.2 ± 2.8; P = 0.009), while isovolumetric relaxation time (101.9 ± 19.9 ms, 85.7 ± 15.2 ms; P < 0.001), and ejection time was longer (101.9 ± 19.9 ms, 85.7 ± 15.2 ms; P = 0.077) and Mitral E/ lateral wall E ratio (E/E relation) was significantly higher (P = 0.031) in patients with higher left atrial volume index. CONCLUSION: The rate of isovolumetric relaxation time, FMD% and E/E' ratio independently predicted left atrial volume index increase in newly diagnosed hypertension patients.

Comparison of 30-Day MACE between Immediate versus Staged Complete Revascularization in Acute Myocardial Infarction with Multivessel Disease, and the Effect of Coronary Lesion Complexity.

Background and objective: In patients with acute myocardial infarction and multivessel disease, the timing of intervention to non-culprit lesions is still a matter of debate, especially in patients without shock. This study aimed to compare the effect of multivessel intervention, performed at index percutaneous coronary intervention (PCI) (MVI-I) or index hospitalization (MVI-S), on the 30-day results of acute myocardial infarction (AMI), and to investigate the effect of coronary lesion complexity assessed by the Syntax (Sx) score on the timing of multivessel intervention. Materials and methods: We enrolled 180 patients with MVI-I, and 425 patients with MVI-S. The major adverse cardiovascular events (MACE) for this study were identified as mortality, nonfatal myocardial infarction, nonfatal stroke, acute heart failure, ischemia driven revascularization, major bleeding, and acute renal failure developed within 30 days. Results: The unadjusted MACE rates at 30 days were 11.2% and 5% among those who underwent MVI-I and MVI-S, respectively (OR 3.02; 95% confidence interval (CI) 1.51⁻6.02; p=0.002). Associations were statistically significant after adjusting for covariates in the penalized multivariable model (adjusted OR 2.06; 95%CI 1.02⁻4.18; p=0.043), propensity score adjusted multivariable model (adjusted OR 2.46; 95%CI 1.19⁻5.07; p=0.015), and IPW (adjusted OR 2.11; 95%CI 1.28⁻3.47; p=0.041). We found that the Syntax score of lesions did not affect the results. Conclusion: MVI-S was associated with a lower incidence of major adverse cardiovascular events within 30 days after discharge.