QT intervals and heart rate variability in hypertensive patients

Low heart rate variability and increased QT dispersion are risk factors for cardiac mortality in various patient populations. We studied dispersion of QT interval, i.e. an index of inhomogeneity of repolarization, and heart rate variability (HRV) i.e., a measure of cardiac autonomie modulation in 76 essential hypertension cases (45 women, 53.0 ± 11.1 years, body mass index: 25.1 ±1.4 kg/m2) and 70 healthy cases (42 women, 54.0 ±10.2 years, body mass index: 25.5 ±1.6 kg/m2,/? > 0.05). QT-corrected QT intervals and their dispersions were significantly higher in the hypertensive group (p 50 msec (p = 0.005), HRV triangular index (p - 0.007), the square root of the mean squared differences of successive RR intervals (p = 0.011), and the high frequency (HF, 0.16-0.40 Hz, p< 0.0001) part of the frequency domain measure of HRV were all decreased, whereas the low frequency (LF, 0.04-0.15 Hz, p = 0.013) part of the frequency domain measures and LF/HF ratio (p < 0.0001) were increased in hypertensive cases. Time domain and the HF part of frequency domain measures of heart rate variability showed an inverse relation with the increased levels of both systolic and diastolic blood pressures and Lown grading system of ventricular rhythm problems, whereas LF and LF / HF showed direct relations with high levels of systolic and diastolic blood pressures and high Lown grade ventricular rhythm problems. The measures of heart rate variability apart from LF and LF / HF were inversely related with the QT intervals and dispersions, whereas LF / HF was directly related with them. Therefore, we conclude that the levels of both systolic and diastolic blood pressures are related to the generation of ventricular rhythm problems either via increasing left ventricular mass which results in an increase in QT parameter measurements, or by altering heart rate variability measures indicating a disturbance in cardiac autonomie balance in essential hypertension

Coronary artery disease and infection with chlamydia pneumonia

The association between chlamydia pneumonia and coronary artery disease is well documented, however less is known about the correlation between chlamydia pneumonia infection and blood inflammatory markers or lipid levels. In 100 patients with proven coronary artery disease (25 females, 61.0 + 4.0 years old), and 60 healthy volunteer control cases (15 females, 60.6 ±3.4 years old), anti chlamydia pneumonia IgG, blood lipid, C-reactive protein and fibrinogen levels were detected. In cases with coronary artery disease seropositivity for IgG antibodies to chlamydia pneumonia (74% versus 34%, p < 0.0001 ), C-reactive protein (mg / /) (2.8 ±0.6 versus 1.4 ±0.6, p < 0.0001 ), fibrinogen (mg / d/) (317.4 ±38.2 versus 256.2 ±34.5, p < 0.0001 ), triglycéride (mg/dl) (217.5 ±39.0 versus 191.0 + 25.9, p <0.0001), LDL-cholesterol (mg /dl) (126.9+ 19.2 versus 110.6± 19.5, p< 0.0001) levels and total cholesterol / HDL-cholesterol ratio (7.7 ±1.8 versus 4.4 + 1.2, p < 0.0001) were higher but the level of HDL-cholesterol (mg/dl) (26.4±6.7 versus 47.0 ±11.2, p< 0.0001) was lower. The levels of total cholesterol did not differ between the two groups (/? = 0.9). Levels of triglycéride (r = 0.60, p< 0.00001), LDL-cholesterol (r = 0.27, p = 0.0004), C-reactive protein (r = 0.69, p < 0.00001), fibrinogen (r = 0.60, p<0.00001) and total cholesterol /HDLcholesterol ratio (r = 0.74, p< 0.00001) had a direct relation, but the level of HDL-cholesterol had a negative (r = -0.80, p< 0.00001) relation with the seropositivity for chlamydia pneumonia. As a result, seropositivity for IgG antibodies to chlamydia pneumonia is considered as a risk factor for coronary artery disease by its association with the atherogenic lipid profile and procoagulant activity

Effect of insulin resistance on left ventricular structural changes in hypertensive patients

Both left ventricular (LV) hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth promoting effect on cardiomyocytes rather than affecting the LV internal diameter. The purpose of this study was to examine the effect of IR on LV geometry. We enrolled 105 patients (71 females, mean age, 49.2 ± 13.6 years) with recently diagnosed and untreated hypertension (blood press > 140 and/or 90 mmHg, fasting glucose < 110 mg/dL), and grouped them as normal (N) (39 patients, 26 females, mean age, 48.5 ± 14.7 years) if all M-mode echocardiographic measurements were within normal limits, concentric remodeling (CR) (22 patients, 15 females, mean age, 50.5 ± 14.8 years) if relative wall thickness was increased but left ventricular mass index (LVMI) was normal, concentric hypertrophy (CH) (13 patients, 9 females, mean age, 50.3 ± 10.8 years) if both ventricular thicknesses and the LVMI were increased, and eccentric hypertrophy (EH) (31 patients, 21 females, mean age, 48.6 ± 12.9 years) if ventricular thicknesses were normal, but LVMI was increased. Transthoracic echocardiography was performed in all subjects, and interventricular septal thickness (IVS), posterior wall thickness (PWT), sum of wall thickness (SWT), left ventricular end-diastolic internal diameter (LVED), relative wall thickness (RWT), and LVMI were recorded. Blood samples for routine biochemical examination and fasting insulin levels were obtained and then the homeostasis model assessment (HOMA) index was calculated by the formula: HOMA Index = Fasting Blood Glucose (mg/dL) × Immunoreactive Insulin (μU/mL)/405, for the assessment of IR. There were no significant differences among the groups with respect to age, blood pressure (BP) levels, fasting blood glucose (FBG), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC), or triglyceride (TG) levels. Insulin levels were significantly higher in the CR and CH groups in comparison with the N group (P = 0.004), and the HOMA index was higher in the CH group compared to the N group (P = 0.024). In Pearson's correlation analysis, insulin was found to be directly correlated with IVS (r = 0.29, P = 0.002), SWT (r = 0.25, P = 0.009), and RWT (r = 0.33, P = 0.0001). The HOMA index was also directly correlated with IVS (r = 0.33, P = 0.001), SWT (r = 0.29, P = 0.002), and RWT (r = 0.29, P = 0.003). Cardiac changes in hypertensive patients include increased LVMI and altered LV geometry. The concentric LV geometry seen in hypertensive patients might be mediated, at least in part, by increased insulin levels and the HOMA index. Copyright © 2006 by the International Heart Journal Association

Effects of ivabradine therapy on heart failure biomarkers

Background: Heart rate (HR) reduction is associated with improved outcomes in patients with heart failure (HF) and biomarkers can be a valuable diagnostic tool in HF management. The primary aim of our study was to evaluate the short-term (6 months) effect of ivabradine on N-terminal pro B-type natriuretic peptide (NT-proBNP), CA-125, and cystatin-C values in systolic HF outpatients, and secondary aim was to determine the relationship between baseline HR and the NT-proBNP, CA-125, cystatin-C, and clinical status variation with ivabradine therapy. Methods: Ninety-eight patients (mean age: 65.81 ± 10.20 years; 33 men), left ventricular ejection fraction &lt; 35% with Simpson method, New York Heart Association (NYHA) class II–III, sinus rhythm and resting HR &gt; 70/min, optimally treated before the study were included. Among them, two matched groups were formed: the ivabradine group and the control group. Patients received ivabradine with an average (range of 10–15) mg/day during 6 months of follow-up. Blood samples for NT-proBNP, CA-125, and cystatin-C were taken at baseline and at the end of a 6-month follow-up in both groups. Results: There was a significant decrease in NYHA class in the ivabradine group (2.67 ± ± 0.47 vs. 1.85 ± 0.61, p &lt; 0.001). When ivabradine and control groups were compared, a significant difference was also found in NHYA class 6 months later (p = 0.013). A significant decrease was found in HR in the ivabradine and control groups (84.10 ± 8.76 vs. 68.36 ± ± 8.32 bpm, p = 0.001; 84.51 ± 10 vs. 80.40 ± 8.3 bpm, p = 0.001). When both groups were compared, a significant difference was also found in HR after 6 months (p = 0.001). A significant decrease was found in cystatin-C (2.10 ± 0.73 vs. 1.50 ± 0.44 mg/L, p &lt; 0.001), CA-125 (30.09 ± 21.08 vs. 13.22 ± 8.51 U/mL, p &lt; 0.001), and NT-proBNP (1,353.02 ± 1,453.77 vs. 717.81 ± 834.76 pg/mL, p &lt; 0.001) in the ivabradine group. When ivabradine and control groups were compared after 6 months, a significant decrease was found in all HF parameters (respectively; cystatin-C: p = 0.001, CA-125: p = 0.001, NT-proBNP: p = 0.001). Creatinine level was significantly decreased and glomerular filtration rate (GFR) was significantly increased in the ivabradine group (1.02 ± 0.26 vs. 0.86 ± 0.17, creatinine: p = 0.001; 79.26 ± 18.58 vs. 92.48 ± 19.88, GFR: p = 0.001). There was no significant correlation between NYHA classes (before and after ivabradine therapy) and biochemical markers, or HR. Conclusions: In the outpatients with systolic HF, persistent resting HF &gt; 70/min with optimal medical therapy, the NT-proBNP, CA-125, and cystatin-C reductions were obtained with ivabradine treatment. Measurement of NT-proBNP, CA-125, and cystatin-C may prove to be useful in biomarker panels evaluating ivabradine therapy response in HF patients.

The association between coronary flow rate and impaired heart rate recovery in patients with metabolic syndrome: A preliminary report

Background: The aim of this study is to evaluate heart rate recovery (HRR) and association between coronary flow rate and HRR in patients with metabolic syndrome (MS) who had morphologically normal coronary angiogram.Methods: Study population included 43 patients with MS and 37 control subjects without MS. All patients were selected from individuals who had recently undergone coronary angiography in our hospital and were diagnosed as having angiographically normal coronary arteries. Exercise stress test results obtained prior to coronary angiography were evaluated for calculating HRR and other parameters. In addition, coronary flow was objectively evaluated for each major coronary artery in each subject using TIMI frame count method.Results: All HRR values calculated were detected significantly lower in MS group compared to controls (HRR first: 32 ± 9 vs. 37 ± 10; p = 0.01, second: 46 ± 11 vs. 52 ± 11; p = 0.03, third: 51 ± 12 vs. 59 ± 12; p = 0.00, fourth: 54 ± 13 vs. 61 ± 2; p = 0.02). TIMI frame counts for each major epicardial coronary artery and mean TIMI frame count were also found to be significantly higher in MS group compared to controls (left anterior descending artery:51 ± 24 vs. 39 ± 15; p = 0.009, left circumflex artery: 32 ± 11 vs. 24 ± 7; p = 0.001, right coronary artery: 33 ± 14 vs. 24 ± 10; p = 0.003, mean TIMI frame count: 38 ± 15 vs. 29 ± 9;p = 0.002). Additionally, significant negative correlations were also detected between HRR first minute and coronary TIMI frame count values in patients with MS. None of MS parameters did not affect HRR values, however mean TIMI frame count independently associated with HRR first minute (p = 0.04) in patients with MS.Conclusions: Impaired coronary blood flow occurring in MS might be a clue of autonomic dysfunction in addition to previously known endothelial dysfunction.

Do female patients with metabolic syndrome have masked left ventricular dysfunction?

Objective: Metabolic syndrome (MS) is a condition, which is recognized as raising the risk of cardiovascular disease. The aim of our study is to estimate the left ventricular functions by atrioventricular plane displacement (AVPD), myocardial performance index (MPI) and conventional methods in patients with MS who were diagnosed according to NCEP (ATP III) criteria. Methods: Fifty-three female patients with MS (mean age 53.1 ± 6.9 years) and 30 healthy female subjects (mean age 52.8 ± 6.3 years, p>0.05) underwent complete echocardiographic assessment. All of the subjects had no heart and pulmonary diseases. The systolic mitral AVPD was recorded at 4 sites (septal, lateral, anterior, and posterior) by M-mode echocardiography and left ventricle ejection fraction (LVEF) was calculated from the AVPD-mean (EF-AVPD). The LVEF was also established by biplane Simpson's (EF-2D) and Teichholz's methods (EF-T). Left ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time) / aortic ejection time by Doppler echocardiography. Results: Patients with MS showed mild left ventricular diastolic dysfunction (DD) in comparison to healthy subjects. The EF-2D and EF-T in patients with MS and healthy subjects were not different significantly and were within normal limits. Patients with MS showed LV global dysfunctions compared to healthy subjects (MPI: 0.56±0.12 and 0.46±0.11 respectively, p<0.01). Both the septal, anterior, lateral and posterior part of the atrioventricular plane values and also AVPD-mean during systole were statistically lower in patients with MS (12.85±1.76 mm) as compared with controls (14.65±2.19 mm, p<0.05). The EF-AVPD in patients with MS was statistically lower (65.58±11.95%) as compared with healthy subjects (74.45±11.07%, p<0.01). Conclusion: Female patients with MS had both left ventricular DD and a global dysfunction with an increased MPI. The EF-2D and EF-T were not different significantly between patients and controls, but patients with MS had a relatively reduced EF-AVPD. The AVPD method may indicate a systolic dysfunction with a relatively lower AVPD-mean and relatively lower EF-AVPD. The presence of global dysfunction in patients with MS may lead to heart failure

Evaluation of heart rate variability in patients with coronary artery ectasia and coronary artery disease

Objective: The present study compared heart rate variability (HRV) parameters in patients with coronary artery ectasia (CAE) and coronary artery disease (CAD). Methods: The study population consisted of 60 consecutive patients with CAE (14 women; mean age 51.63±7.44 years), 60 consecutive patients with CA (15 women; mean age 53.67±9.31 years), and 59 healthy individuals (13 women; mean age 52.85±8.19 years). Electrocardiograms, 24-hour Holter analyses, and routine biochemical tests were performed, and clinical characteristics were evaluated. Coronary angiography images were analyzed. Time-domain HRV parameters, including the standard deviation (SD) of normal-to-normal intervals (SDNN) and the root mean square of difference in successive normal-tonormal intervals (RMSSD) were evaluated, as were frequencydomain HRV parameters including low-frequency (LF), very lowfrequency (VLF), high-frequency (HF), the proportion derived by dividing low- and high-frequency (LF/HF), and total power (TP). Results: SDNN was lower in both the CAE and CAD groups, compared to the healthy group (140.85±44.21, 96.51±31.28, and 181.05±48.67, respectively). A significant difference in RMSSD values among the groups was determined (p=0.004). Significantly decreased VLF and HF values were found in the CAE group, compared with the healthy group (VLF p<0.001; HF, p=0.007). TP, VLF, and HF values were significantly lower (p<0.001, p<0.001, and p<0.001, respectively), but LF and LF/ HF values were significantly higher (p<0.001 for both) in the CAD group than in the healthy group. TP values were significantly higher (p<0.001), and LF and LF/HF values were lower in the CAE group, compared with the CAD group (p<0.001 for both). Conclusion: A decrease in vagal modulation or an increase in sympathetic activity of cardiac function, assessed by HRV analysis, is worse in patients with CAD than in patients with CAE. © 2016 Turkish Society of Cardiology

Manual thrombus aspiration and the improved survival of patients with unstable angina pectoris treated with percutaneous coronary intervention (30 months follow-up)

The clinical effect of intracoronary thrombus aspiration during percutaneous coronary intervention in patients with unstable angina pectoris is unknown. In this study, we aimed to assess how thrombus aspiration during percutaneous coronary intervention affects in-hospital and 30-month mortality and complications in patients with unstable angina pectoris. We undertook an observational cohort study of 645 consecutive unstable angina pectoris patients who had performed percutaneous coronary intervention from February 2011 to March 2013. Before intervention, 159 patients who had culprit lesion with thrombus were randomly assigned to group 1 (thrombus aspiration group) and group 2 (stand-alone percutaneous coronary intervention group). All patients were followed-up 30 months until August 2015. Thrombus aspiration was performed in 64 patients (46%) whose cardiac markers (ie, creatinine kinase [CK-MB] mass and troponin T) were significantly lower after percutaneous coronary intervention than in those of group 2 (CK-MB mass: 3.801.11 vs 4.230.89, P=0.012; troponin T: 0.0120.014 vs 0.0180.008, P=0.002). Left ventricular ejection fraction at 6, 12, and 24 months postintervention was significantly higher in the group 1. During a mean followup period of 28.876.28 months, mortality rates were 6.3% in the group 1 versus 12.9% in the group 2. Thrombus aspiration was also associated with significantly less long-term mortality in unstable angina pectoris patients (adjusted HR: 4.61, 95% CI: 1.16-18.21, P=0.029). Thrombus aspiration in the context of unstable angina pectoris is associated with a limited elevation in cardiac enzymes during intervention that minimises microembolization and significantly improves both of epicardial flow and myocardial perfusion, as shown by angiographic TIMI flow grade and frame count. Thrombus aspiration during percutaneous coronary intervention in unstable angina pectoris patients has better survival over a 30-month follow-up period. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved

Markers of chronic infection and inflammation. Are they important in cases with chronic coronary heart disease

The human cytomegalovirus plays a causal role in atherosclerosis etiology, but it is discussed as controversial. We conducted a case control study to investigate whether previous infection with cytomegalovirus is associated with coronary heart disease and markers of systemic inflammation, because systemic inflammation may play a role in atherosclerosis too. We also studied the correlation between anti-cytomegalovirus antibody titer and coronary artery disease. The study involved 150 cases (45 females, mean age ± SD is 58.73 ± 7.68 years) with a documented coronary heart disease and 160 healthy volunteers (50 females, mean age ± SD is 57.82 ± 7.68, p > 0.05). Cytomegalovirus serology was performed to determine the presence of specific IgG antibodies and titers of the anti-cytomegalovirus IgG antibodies. In addition, C-Reactive protein levels were determined for each case. The prevalance of specific antibodies to cytomegalovirus was 57.30% for the patients and 56% for the controls (p = 0.39). But higher levels of anti-cytomegalovirus IgG antibody titer (> 1/ 800) were seen in the patient group (28.6% versus 10%, p = 0.0000). Mean value of C-reactive protein was higher in the patient group (2.99 ± 0.92 mg/l versus 1.79 ± 0.51 mg/l, p = 0.0000), and there was a linar correlation with the high antibody titers and the level of C-reactive protein (r = 0.35, p = 0.0000). These findings support that not the seropositivity of the population but rather the titer of anti-cytomegalovirus antibody and the levels of C-reactive protein could predict patients with a high risk of coronary heart disease

preconditioning

Potentially hazardous short ischemic episodes increase the tolerance of myocardium to ischemia paradoxically. This condition decreases the infarct area markedly caused by a longer duration of coronary occlusion. This phenomenon is known as 'ischemic preconditioning' and its powerful cardioprotective effect has been shown in experimental and clinical studies. Ischemic preconditioning decreases cardiac mortality markedly by preventing the development of left ventricular dysfunction and ventricular and supraventricular arrhythmias after acute myocardial infarction. Ischemia-induced opening of ATP-sensitive potassium channels and synthesis of stress proteins via activation of adenosine, bradykinin and prostaglandin receptors seem to be the possible mechanisms. By understanding the underlying mechanisms of ischemic preconditioning, it may be possible to develop new pharmacologic agents that cause ischemic preconditioning with antiischemic and antiarrhythmic properties without causing myocardial ischemia