Cardiac autonomic involvement in Huntington's disease.

INTRODUCTION: Huntington's disease (HD) is known as a neurodegenerative disease with movement disorder and cognitive impairment; autonomic involvement is also becoming common in some recent studies. The aim of this study is to demonstrate the presence of cardiac autonomic involvement in HD patients. METHOD: Time and frequency domain parameters obtained from the 24-h Holter ECG(hECG) were compared between 20 HD patients and 20 healthy control subjects. RESULTS: Fourteen HD patients had tachycardia, bradycardia, and extra beats. Interval between two heartbeats, normal-to-normal (NN), standard deviation of all normal-to-normal (SDNN), square root of the mean of the sum of the squares of the differences between consecutive N-N intervals in ms (rMSSD), and the ratio of the number of consecutive pairs of N-N intervals that differ by more than 50 ms to the total number of N-N intervals (pNN50) were all significantly higher in the patient group than in the control group during 24-h hECG monitoring. However, hECG monitoring showed that the patient group had significantly higher values of the frequency-domain metrics high frequency (HF) than the control group did (P = 0.003). Very low frequency (VLF) was lower in the patient group (P = 0.009). There was no difference in low frequency (LF) in both groups. In comparison to the control group, LF/HF was much reduced in the patient group (P = 0.001). CONCLUSION: Cardiac disfunction increases, and autonomic functions change in HD, but more comprehensive studies are needed to distinguish sympathetic and parasympathetic involvement.

Can platelet count be controlled with ticagrelor in patients with essential thrombocythaemia? A case series.

Background: Essential thrombocythaemia (ET) is defined as a myeloproliferative neoplasm with a tendency to haemorrhage and thrombosis. Acute coronary thrombosis can be observed in 1 out of 10 patients. The management of ET patients with acute coronary syndrome (ACS) is a complex clinical condition that requires close follow-up. Case summary: Case-1: a 52-year-old female patient with a diagnosis of ET with Janus kinase (JAK)--2 mutation, despite using cytoreductive agents, platelet counts could not be controlled. Platelet counts started to follow a normal course with the ticagrelor treatment given after ACS. Case-2: a 49-year-old female patient who was given ticagrelor treatment after ACS was found to have JAK-2+ ET. The patient whose platelet count returned to normal after ticagrelor treatment was using a cytoreductive agent before the index event. Case-3: a 54-year-old female patient with ET without any genetic mutation. In the patient whose platelet count did not decrease despite ticagrelor treatment and cytoreductive agents given after ACS, platelet counts returned to normal with interferon therapy. Discussion: Platelet counts returned to the normal range with ticagrelor treatment given after ACS in patients with JAK+ ET. Monitoring platelet reduction in JAK+ patients with P2Y12 inhibition is thought to be important for new treatment options.

Effects of chronic obstructive pulmonary disease on coronary atherosclerosis.

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.

The relationship between Chlamydophila pneumoniae IgG titer and coronary atherosclerosis.

BACKGROUND: The role of Chlamydophila pneumoniae (CP) in the progression of atherosclerosis is controversial. Also no sufficient angiographic study is available about the impact of CP infection on severity and intensity of coronary atherosclerosis. We investigated the relation between CP IgG antibody titers and severity and intensity of coronary atherosclerosis METHODS: The study population consisted of 516 consecutive patients who underwent a coronary angiography. The group included 353 patients who had coronary artery disease; a control group included 163 subjects with angiographically proven normal coronary arteries. Chlamydophila pneumoniae IgG antibody titers were measured by an enzyme immunoassay method in all patients. Gensini scores and extent scores were used to evaluate the angiographic extent and severity of atherosclerosis. RESULTS: The mean value of IgG antibody titer was 44.3 +/- 28.8 IU/mL in the patients and 39.8 +/- 27.4 IU/mL in the control group (p = 0.14). There was no statistically significant correlation between the Gensini scores, extent scores and CP IgG titers (Gensini score: r = +0.103, p = 0.07, extent score: r = +0.110, p = 0.31). When we grouped the patients as high (> 50 IU/mL) and low (< 50 IU/mL) IgG antibody titers, the number of diseased coronary arteries was higher in patients with high IgG antibody titers (respectively: 2.6 +/- 1.1 vs. 2.2 +/- 0.8, p = 0.01). While the Gensini score was significantly higher in patients with high IgG antibody titers (7.5 +/- 4.0 vs. 6.17 +/- 4.0, p = 0.01), the extent score did not change with IgG titers (29.8 +/- 15.9 vs. 25.8 +/- 15.4, p = 0.08). CONCLUSIONS: In our study, we investigated the relation between CP infection and coronary atherosclerosis and found that CP IgG antibody titers are associated with the severity of coronary stenosis at higher antibody levels. However, there is no association between CP antibody titers and clinical presentation of coronary artery disease. We suggest that CP has limited effect on coronary atherosclerosis.

Effects of intermittent and long-term glucose-insulin-potassium infusion in patients with systolic heart failure.

BACKGROUND: Although single dose and short-term glucose-insulin-potassium (GIK) infusions are known to have positive cardiac effects, the effects of repeated and long-term GIK infusion on left ventricular (LV) systolic function and brain natriuretic peptide (BNP) levels are unknown. OBJECTIVE: To investigate the effects of repeated and long-term GIK infusion on LV systolic function and BNP levels. METHODS: Thirty-three patients diagnosed with ischemic cardiomyopathy were included in the study. Patients were divided into two groups: the GIK group (n=19) and the control group (n=14). GIK solutions (1000 mL 20% dextrose, 60 U insulin and 50 mmol/L KCl) were administered at 1 mL/kg/h for 24 h on the first, third and fifth days. The patients were examined by echocardiography at 24 h, one week and one month after the start of treatment. BNP levels were measured before and after GIK infusion. RESULTS: In the GIK group, baseline ejection fraction (EF) was 29.2+/-10.3%. After one week, EF elevated to 40.8+/-10.8% (P=0.001). The EF after one month (37.1+/-10.9%) was less than the EF in the first week, but it was significantly higher than baseline in the GIK group (P=0.01). However, no significant changes in EF were observed after one week and one month in the control group (P=0.1 and P=0.2, respectively). BNP levels after GIK infusion was significantly lower than baseline level in the GIK group (P=0.01). CONCLUSION: Intermittent and long-term GIK infusion has beneficial effects on LV systolic function in a short and intermediate amount of time. Decrease in BNP levels may indicate effective GIK treatment. Intermittent and long-term GIK infusion could be a promising treatment option in patients with systolic heart failure.

Use of ischemia-modified albumin in diagnosis of coronary artery disease.

OBJECTIVE: The diagnosis of coronary artery disease (CAD) is an important clinical problem. Ischemia-modified albumin (IMA) has been demonstrated to be a helpful marker in detecting myocardial ischemia. In this study, we have investigated the diagnostic importance of IMA in CAD. METHOD AND RESULTS: Fifty patients with chest pain were enrolled in the study. IMA levels were measured on admission and within 30-60 min after exercise by albumin cobalt-binding test. Coronary angiography was performed in all patients after the exercise test. The mean preexercise IMA level was 83+/-27 U/ml in the patient group. IMA levels before the exercise test were similar in both patient and control groups (P>0.05). The mean IMA level in the patient group was, however, higher than in the control group after the exercise test (P=0.001). The sensitivity, specificity and positive and negative predictive values of the postexercise IMA levels >85 in diagnosis of CAD were 78, 73, 0.81 and 0.73%; respectively. Postexercise IMA levels were higher in patients with chest pain, ST depression and downsloping and horizontal ST depression of 2 mm or more. CONCLUSION: IMA levels after the exercise test increased in patients with CAD. Our study results indicate that postexercise IMA levels can be helpful markers in the diagnosis of stable CAD in clinical practice.

Spontaneous coronary artery dissection and pulmonary thromboembolism: a case report.

Spontaneous coronary artery dissection (SCAD) still is a rare cause of acute coronary syndrome. SCAD has been observed in three groups of patients: those with coronary atherosclerosis, peripartal women and idiopathic group. SCAD may be associated with some conditions. We report an unusual association: SCAD and pulmonary thromboembolism.

Cardiovascular effects of carbon monoxide poisoning.

Carbon monoxide (CO) poisoning is an important health problem. Cardiac abnormalities may occur in patients with CO poisoning; however, the severity and duration of cardiac abnormalities are not well known. In this study, cardiac structures and function in CO poisoning were evaluated prospectively. Twenty patients were enrolled in the study. Echocardiographic examination was performed in all patients on admission, at 24 hours, and within the first week. B-type natriuretic peptide and carboxyhemoglobin levels were measured. Patients with increased cardiac markers underwent coronary angiography. Cardiac markers were high in 6 patients. Patients with high cardiac markers had significantly higher carboxyhemoglobin levels and longer exposure to CO. Left ventricular ejection fraction (LVEF) was <45% in 8 patients (group I) on admission and >55% in 7 patients in group I 24 hours after echocardiography. A significant negative correlation was found between B-type natriuretic peptide and LVEF on admission (r = -0.586, p <0.01). The decrease in LVEF was also negatively correlated with carboxyhemoglobin level and CO exposure duration. All angiograms showed normal coronary arteries. In conclusion, despite normal coronary arteries, myocardial dysfunction may occur in patients with CO poisoning. LV systolic function might be normal or mildly to severely impaired. However, most of the myocardial dysfunction dissipates at 24 hours in patients with CO poisoning.

Protective effects of carvedilol against anthracycline-induced cardiomyopathy.

OBJECTIVES: The aim of this study was to determine the protective effect of carvedilol in anthracycline (ANT)-induced cardiomyopathy (CMP). BACKGROUND: Despite its broad effectiveness, ANT therapy is associated with ANT-induced CMP. Recent animal studies and experimental observations showed that carvedilol prevented development of CMP due to chemotherapeutics. However, there is no placebo-controlled clinical trial concerning prophylactic carvedilol use in preventing ANT-induced CMP. METHODS: Patients in whom ANT therapy was planned were randomized to administration of carvedilol or placebo. We enrolled 25 patients in carvedilol and control groups. In the carvedilol group, 12.5 mg once-daily oral carvedilol was given during 6 months. The patients were evaluated with echocardiography before and after chemotherapy. Left ventricular ejection fraction (EF) and systolic and diastolic diameters were calculated. RESULTS: At the end of 6 months of follow-up, 1 patient in the carvedilol group and 4 in the control group had died. Control EF was below 50% in 1 patient in the carvedilol group and in 5 in the control group. The mean EF of the carvedilol group was similar at baseline and control echocardiography (70.5 vs. 69.7, respectively; p = 0.3), but in the control group the mean EF at control echocardiography was significantly lower (68.9 vs. 52.3; p < 0.001). Both systolic and diastolic diameters were significantly increased compared with basal measures in the control group. In Doppler study, whereas E velocities in the carvedilol group decreased, E velocities and E/A ratios were significantly reduced in the control group. CONCLUSIONS: Prophylactic use of carvedilol in patients receiving ANT may protect both systolic and diastolic functions of the left ventricle.