Polychronis Dilaveris

Simple electrocardiographic markers for the prediction of paroxysmal idiopathic atrial fibrillation

BACKGROUND The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (PAF). METHODS To search for possible electrocardiographic markers that could serve as predictors of idiopathic PAF, we measured the maximum P-wave duration (P maximum) and the difference between the maximum and the minimum P-wave duration (P dispersion) from the 12-lead surface electrocardiogram of 60 patients with a history of idiopathic PAF and 40 age-matched healthy control subjects. RESULTS P maximum and P dispersion were found to be significantly higher in patients with idiopathic PAF than in control subjects. A P maximum value of 110 msec and a P dispersion value of 40 msec separated patients from control subjects, with a sensitivity of 88% and 83% and a specificity of 75% and 85%, respectively. CONCLUSIONS P maximum and P dispersion are simple electrocardiographic markers that could be used for the prediction of idiopathic PAF.

Effects of Ischemia on P Wave Dispersion and Maximum P Wave Duration During Spontaneous Anginal Episodes

P wave dispersion (P dispersion), defined as the difference between the maximum and the minimum P wave duration, and maximum P wave duration (P maximum) are electrocardiographic (ECG) markers that have been used to evaluate the discontinuous propagation of sinus impulses and the prolongation of atrial conduction time, respectively. To study the effects of myocardial ischemia on P dispersion and P maximum, 95 patients with coronary artery disease (CAD) and typical angina pectoris and 15 controls with anginalike symptoms underwent 12‐lead surface ECG during and after the relief of pain. During pain and during the asymptomatic period, P maximum and P dispersion were calculated from the averaged complexes of all 12 leads. P dispersion increased significantly during spontaneous angina (45 ± 17 ms) compared to the asymptomatic period (40 ± 15 ms), P < 0.001 only in the patient group. Both P maximum and P dispersion showed higher values during angina in those patients who developed diffuse ischemia, as estimated with ST segment changes in multiple ECG leads. P dispersion showed higher values during the anginal episode in patients with left ventricular dysfunction, independently of the presence of a previous myocardial infarction. Atrial conduction abnormalities, as estimated with P maximum and particularly P dispersion, are significantly influenced by myocardial ischemia in patients with CAD and spontaneous angina.

Improved Detection of Coronary Artery Disease by Exercise Electrocardiography with the Use of Right Precordial Leads

BACKGROUND Exercise electrocardiography is an perfect test for the detection of coronary artery disease. We attempted to improve the diagnostic accuracy of exercise testing as a noninvasive method for the detection of coronary artery disease by using a combination of the left and right precordial leads. METHODS We studied 245 patients (218 men and 27 women) ranging from 32 to 74 years of age (mean [+/-SD], 52+/-8) who underwent treadmill exercise testing, thallium-201 scintigraphy, and coronary arteriography. During exercise testing, each patient had one electrocardiogram recorded with the standard 12 leads and 3 right precordial leads (V3R, V4R, and V5R), with the results for each set of leads recorded and analyzed separately. RESULTS On the basis of coronary arteriography, 34 patients had normal coronary arteries, 85 had single-vessel disease, 84 had two-vessel disease, and 42 had three-vessel disease. The sensitivities of the standard 12-lead exercise electrocardiogram, exercise electrocardiography incorporating right precordial leads, and thallium-201 scintigraphy were 52 percent, 89 percent, and 87 percent, respectively, for the detection of single-vessel disease; 71 percent, 94 percent, and 96 percent for the detection of two-vessel disease; 83 percent, 95 percent, and 98 percent for the detection of three-vessel disease; and 66 percent, 92 percent, and 93 percent for the detection of any coronary artery disease. The specificities of the three methods for the detection of any coronary artery disease were 88 percent, 88 percent, and 82 percent, respectively. CONCLUSIONS Use of right precordial leads along with the standard six left precordial leads during exercise electrocardiography greatly improves the sensitivity of exercise testing for the diagnosis of coronary artery disease.

CLimate Impacts on Myocardial infarction deaths in the Athens TErritory: the CLIMATE study

Objective: To evaluate the impact of meteorological variables on daily and monthly deaths caused by acute myocardial infarction (AMI). Methods: All death certificate data from the Athens territory were analysed for AMI deaths in 2001. Daily atmospheric temperature, pressure and relative humidity data were obtained from the National Meteorological Society for Athens for the same year. Results: The total annual number of deaths caused by AMI was 3126 (1953 men) from a population of 2 664 776 (0.117%). Seasonal variation in deaths was significant, with the average daily AMI deaths in winter being 31.8% higher than in summer (9.89 v 7.35, p < 0.001). Monthly variation was more pronounced for older people (mean daily AMI deaths of people older than 70 years was 3.53 in June and 7.03 in December; p < 0.001) and of only marginal significance for younger people. The best predictor of daily AMI deaths was the average temperature of the previous seven days; the relation between daily AMI deaths and seven-day average temperature (R2  =  0.109, p < 0.001) was U-shaped. Considering monthly AMI death rates, only mean monthly humidity was independently associated with total deaths from AMI (R2  =  0.541, p  =  0.004). Conclusion: Ambient temperature is an important predictor of AMI mortality even in the mild climate of a Mediterranean city like Athens, its effects being predominantly evident in the elderly. Mean monthly humidity is another meteorological factor that appears to affect monthly numbers of AMI deaths. These findings may be useful for healthcare and civil protection planning.

Detection of hypertensive patients at risk for paroxysmal atrial fibrillation during sinus rhythm by computer-assisted P wave analysis

OBJECTIVE AND METHODS To determine whether hypertensive patients at risk for paroxysmal atrial fibrillation (AF) could be detected while in sinus rhythm, a computer-based 12-lead surface electrocardiogram was recorded in 50 hypertensive patients with history of paroxysmal AF (group A) and in 60 hypertensive patients without history of AF (group B). The maximum P-wave duration (P(maximum)), the minimum P-wave duration (P(minimum)), P-wave dispersion (Pdispersion = Pmaximum Pminimum), adjusted P-wave dispersion (APdispersion = Pdispersion/square root of the number of measurable leads), mean P-wave duration (mean P) and the standard deviation of the P-wave duration in all measured leads (SDP) were calculated. RESULTS Pdispersion, APdispersion and SDP were significantly higher in group A than in group B (Pdispersion, 52 +/- 19 versus 41 +/- 15 ms, P< 0.001; APdispersion, 15.2 +/- 5.5 versus 11.9 +/- 4.6 ms, P< 0.001; SDP, 16 +/- 5 versus 13 +/- 5 ms, P < 0.001). P(minimum), mean P and left ventricle ejection fraction (LVEF) were significantly lower in group A than in group B (Pminimum, 79 +/- 18 versus 91 +/- 13 ms, P < 0.001; mean P, 108 +/- 18 versus 116 +/- 13 ms, P= 0.005; LVEF, 64 +/- 5 versus 69 +/- 8%, P< 0.001). Pminimum, Pdispersion, mean P, SDP, APdispersion and LVEF were found to be significant univariate predictors of paroxysmal AF, whereas only Pminimum (P< 0.001) remained a significant independent predictor of paroxysmal AF in the multivariate analysis. CONCLUSION Hypertensive patients at risk for paroxysmal AF could be detected while in sinus rhythm by computer-assisted electrocardiographic P-wave analysis.

Beneficial Effects of Statins on Endothelial Dysfunction and Vascular Stiffness

Endothelial dysfunction and increased arterial stiffness are considered independent predictors of cardiovascular risk. Endothelial dysfunction primarily reflects decreased availability of nitric oxide, a critical endothelium-derived vasoactive factor with vasodilatory and anti-atherosclerotic properties. Techniques for assessing endothelial dysfunction include ultrasonographic measurement of flow-mediated vasodilatation of the brachial artery and plethysmographic measurement of forearm blood flow responses to vasoactive agents. Arterial stiffness can be assessed using pulse wave analysis to generate measures of pulse wave velocity, arterial compliance and wave reflection. It has been demonstrated that the preventive effect of statins on coronary events is not only attributed to cholesterol-lowering, but also to various effects on the vascular wall, which include improved endothelial function as well as antioxidant and anti-inflammatory activity. Previous studies have reported improvement of arterial stiffness by the antioxidant and anti-inflammatory effects of statin therapy in patients with or without hypercholesterolemia. The present review considers the pathophysiology underlying endothelial dysfunction and increased arterial stiffness associated with atherosclerotic disease and the beneficial effects of statins on these markers of atherosclerosis.

P Wave Dispersion: A Valuable Electrocardiographic Marker for the Prediction of Paroxysmal Lone Atrial Fibrillation

Background: The prolongation of atrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiological characteristics in patients with paroxysmal atrial fibrillation.

Dose-dependent effects of short term atorvastatin treatment on arterial wall properties and on indices of left ventricular remodeling in ischemic heart failure

OBJECTIVES Statins, beyond their lipid lowering role, exert beneficial effect on endothelial function in patients with atherosclerosis. Aim of the present study was to examine the short term pleiotropic effects of different doses of atorvastatin treatment, on endothelial function, arterial stiffness and indices of left ventricular remodeling in heart failure (HF) patients. METHODS We studied the effect of 4 weeks administration of atorvastatin in 22 patients with ischemic HF. The study was carried out on two separate arms, one with atorvastatin 40 mg/d and one with atorvastatin 10 mg/d (randomized, double-blind, cross-over design). Endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery and arterial stiffness by augmentation index (AIx). Serum levels of matrix metalloproteinase-9 (MMP-9) and intracellular adhesion molecule-1 (sICAM-1) were measured as biomarkers of left ventricular remodeling and endothelial function, respectively, while, b-type natriuretic peptide (BNP) was measured as a marker of left ventricular function. RESULTS Compared to baseline, atorvastatin 40 mg/d significantly improved FMD values (3.18 ± 3.03% vs. 5.98 ± 2.49%, p = 0.001) and AIx values (25.98 ± 8.55% vs. 23.09 ± 8.87%, p = 0.046). In addition, compared to baseline measurements, treatment with atorvastatin 40 mg/d resulted in significantly decreased levels of serum logMMP-9 levels (2.47 ± 0.23 ng/ml vs. 2.39 ± 0.24 ng/ml, p = 0.04) and of logICAM-1 levels (2.46 ± 0.13 ng/ml vs. 2.37 ± 0.16 ng/ml, p < 0.001). No significant changes were found after treatment with atorvastatin 10 mg/d in the aforementioned parameters. CONCLUSIONS Short term treatment with 40 mg/d of atorvastatin exerts beneficial impact on arterial wall properties and on indices of left ventricle remodeling in heart failure patients.

Primary prevention of sudden cardiac death in a nonischemic dilated cardiomyopathy population: reappraisal of the role of programmed ventricular stimulation.

Background— We considered the role of programmed ventricular stimulation in primary prevention of sudden cardiac death in an idiopathic dilated cardiomyopathy population. Methods and Results— One hundred fifty-eight patients with idiopathic dilated cardiomyopathy underwent programmed ventricular stimulation. Ventricular tachycardia/ventricular fibrillation was triggered in 44 patients (group I, 27.8%) versus 114 patients (group II), where ventricular tachycardia/ventricular fibrillation was not induced. Sixty-nine patients with idiopathic dilated cardiomyopathy underwent implantable cardioverter-defibrillator (ICD) implantation: 41/44 in group I and 28/114 in group II. The major end points of the study were overall mortality and appropriate ICD activation. Overall mortality during the 46.9 months of mean follow-up was not significantly different between the 2 groups. Patients with left ventricular ejection fraction ≤35% (n=119) demonstrated a higher overall mortality rate compared with the patients with left ventricular ejection fraction >35% (n=39; 16.8% versus 10.3%, log-rank P =0.025). Advanced New York Heart Association class (III and IV versus I and II) was the single independent and strongest prognostic factor of overall mortality (hazard ratio, 11.909; P <0.001; confidence interval, 3.106–45.65), as well as of cardiac mortality (hazard ratio, 14.787; P =0.001; confidence interval, 2.958–73.922). Among ICD recipients, ICD activation rate was significantly higher in group I compared with group II (30 of 41 patients–73.2% versus 5 of 28 patients–17.9%; log-rank P =0.001), either in the form of antitachycardia pacing (68.3% versus 17.9%; log-rank P =0.001) or in the shock delivery form (51.2% versus 17.9%; log-rank P =0.05). Induction of ventricular tachycardia/ventricular fibrillation during programmed ventricular stimulation in contrast to left ventricular ejection fraction was the single independent prognostic factor for future ICD activation (hazard ratio, 4.195; P =0.007; confidence interval, 1.467–11.994). Conclusions— Inducibility of ventricular tachycardia/ventricular fibrillation was associated with an increased likelihood of subsequent ICD activation and sudden cardiac death surrogate.Background—We considered the role of programmed ventricular stimulation in primary prevention of sudden cardiac death in an idiopathic dilated cardiomyopathy population. Methods and Results—One hundred fifty-eight patients with idiopathic dilated cardiomyopathy underwent programmed ventricular stimulation. Ventricular tachycardia/ventricular fibrillation was triggered in 44 patients (group I, 27.8%) versus 114 patients (group II), where ventricular tachycardia/ventricular fibrillation was not induced. Sixty-nine patients with idiopathic dilated cardiomyopathy underwent implantable cardioverter-defibrillator (ICD) implantation: 41/44 in group I and 28/114 in group II. The major end points of the study were overall mortality and appropriate ICD activation. Overall mortality during the 46.9 months of mean follow-up was not significantly different between the 2 groups. Patients with left ventricular ejection fraction ⩽35% (n=119) demonstrated a higher overall mortality rate compared with the patients with left ventricular ejection fraction >35% (n=39; 16.8% versus 10.3%, log-rank P=0.025). Advanced New York Heart Association class (III and IV versus I and II) was the single independent and strongest prognostic factor of overall mortality (hazard ratio, 11.909; P<0.001; confidence interval, 3.106–45.65), as well as of cardiac mortality (hazard ratio, 14.787; P=0.001; confidence interval, 2.958–73.922). Among ICD recipients, ICD activation rate was significantly higher in group I compared with group II (30 of 41 patients–73.2% versus 5 of 28 patients–17.9%; log-rank P=0.001), either in the form of antitachycardia pacing (68.3% versus 17.9%; log-rank P=0.001) or in the shock delivery form (51.2% versus 17.9%; log-rank P=0.05). Induction of ventricular tachycardia/ventricular fibrillation during programmed ventricular stimulation in contrast to left ventricular ejection fraction was the single independent prognostic factor for future ICD activation (hazard ratio, 4.195; P=0.007; confidence interval, 1.467–11.994). Conclusions—Inducibility of ventricular tachycardia/ventricular fibrillation was associated with an increased likelihood of subsequent ICD activation and sudden cardiac death surrogate.

Improved myocardial performance during repetitive exercise testing: The role of extracellular superoxide dismutase activity in a model of exercise-induced myocardial preconditioning

BACKGROUND The aim of this study was to investigate whether endogenous antioxidant defense is involved in adaptation to myocardial ischemia in patients with coronary artery disease and severe exercise-induced myocardial ischemia. METHODS Fifty patients, aged 50 to 72 years (mean, 58 +/- 6 years), with positive exercise test results underwent 4 treadmill exercise tests. Thallium-201 scintigraphy was performed during the first and the fourth testing. The second, the third, and the fourth tests were performed the next day. The time interval between the second and the third test was 15 minutes, and between the third and the fourth test, the interval was 45 minutes. Extracellular superoxide dismutase activity was measured just before and at the peak of the first and the fourth exercise test. RESULTS The patients were divided in 2 groups according to the extent of myocardial ischemia at peak exercise of the fourth test compared with the first test. Most of the patients studied (37/50) showed improved myocardial performance during the last of the sequential exercise tests, as demonstrated with the studied exercise parameters and the extent of myocardial ischemia in thallium-scintigraphy. Extracellular superoxide dismutase activity before the last exercise test was found to be significantly increased only in the patients who had improved myocardial performance at the last of the sequential exercise tests. CONCLUSION The beneficial effects of sequential episodes of exercise-induced myocardial ischemia seem to be strongly related to extracellular superoxide dismutase activity. Although there is still lack of direct evidence, our data support the theory that the favorable adaptation to repetitive exercise may represent an aspect of the clinical relevance of ischemic preconditioning in humans.