Hypertension and arrhythmia: blood pressure control and beyond.

Arrhythmias are common problems in hypertensive patients. The presence and complexity of both supraventricular and ventricular arrhythmias may influence morbidity, mortality, as well as the quality of life of patients. Diastolic dysfunction of the left ventricle, left atrial size and function, and left ventricular hypertrophy have been suggested as the underlying risk factors for supraventricular and ventricular arrhythmias in hypertensives. Recently, several non-invasive electrocardiographic parameters have been defined and widely investigated to identify the hypertensive patient at risk for the development of arrhythmias. These parameters include signal averaged analysis of P wave, QT interval dispersion, heart rate variability, ventricular late potentials and T wave morphology analysis. The aim of this review was to evaluate the relationships between high blood pressure, ventricular and supraventricular arrhythmias, relevant non-invasive cardiac parameters for risk assessment in hypertensive patients and the effects of blood pressure control.

What is the optimal evaluation time of the QT dispersion after acute myocardial infarction for the risk stratification?

The sequential changes of the corrected QT dispersion (QTcD) were studied in 136 patients 1 day to 30 days after a transmural acute myocardial infarction (AMI) to investigate the optimal measurement time of QT dispersion for risk stratification. The study group included 136 patients (89 men; mean age, 57+/-10 years) with transmural AMI who were treated with thrombolytics (Tr+ group, n = 73) or not (Tr- group, n = 63) and 65 healthy controls (43 men; mean age, 56+/-7 years). Fourteen patients in whom ventricular tachycardia (VT), ventricular fibrillation (VF), or sudden cardiac death developed during the 30-day period were also evaluated as major cardiac arrhythmia (MCA) group. ECGs were obtained for each patient on days 1, 3, 5, 10, 15, and 30 after AMI. QTc dispersion in patients with AMI (for every period of QTcD after MI) was significantly more prolonged than in normal controls (49.3+/-16.3 ms) (p<0.001). QTcD was significantly greater in patients without thrombolytics than in patients with thrombolytics for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p<0.001). The mean of QTcD was significantly greater in patients with MCA than in patients without MCA group for every period (days 1, 3, 5, 10, 15, and 30) of QTcD after MI (p < 0.05). Maximal QTcD was seen on day 10 (p < 0.05 1st vs day 10 for each group) after myocardial infarction, and then reached a plateau for an each group. The ideal time to measure the QTD for risk stratification is at least 10 days after AMI.

The diagnostic value of 12-lead electrocardiogram in predicting infarct-related artery and right ventricular involvement in acute inferior myocardial infarction.

BACKGROUND: The aim of the present study was to investigate the predictive value of presentation and 24-hour electrocardiograms in defining the infarct-related artery (IRA), its lesion segment, and the right ventricular involvement in acute inferior myocardial infarction (MI). METHODS: One hundred forty-nine patients with acute inferior MI were included. Infarct-related artery, its lesion segment, and the validity of new ECG criteria for the diagnosis of right ventricular MI (RVMI) were investigated by means of criteria obtained from admission and 24- hour ECGs. RESULTS: The presence of ST-segment elevation in lead III > lead II criterion (Criterion 1) and ST-segment depression in lead I > lead aVL criterion (Criterion 2) from admission ECG defined the right coronary artery (RCA) as IRA with a sensitivity of 64% and a specificity of 100%. These two criteria also defined the proximal or mid lesions in RCA as culprit lesions (sensitivity of 99%, specificity of 96%). Absence of these two criteria indicated Cx as IRA with a sensitivity of 50% and a specificity of 97%. The depth of Q wave in lead III > lead II criterion (Criterion 3) had no value for discrimination of IRA, but the width of Q wave in lead III > lead II criterion (Criterion 4) supported the RCA to be IRA with a sensitivity of 60% and a specificity of 61% (Criteria 3 and 4 were obtained from 24-hour ECGs). The finding of Criterion 1 plus Criterion 5 (ST elevation in V(1) but no ST elevation in V2) on admission ECG had a sensitivity of 63% and a specificity of 99% in the diagnosis of RVMI. CONCLUSION: We concluded that 12-lead ECG is a cheap, easy, and readily obtainable diagnostic approach in discrimination of IRA and its culprit lesion segment. However, despite high specificity, due to moderate degree sensitivity, its value for the diagnosis of RVMI is questionable.

Cytomegalovirus, Chlamydia pneumoniae, and Helicobacter pylori IgG antibodies and restenosis after stent implantation: an angiographic and intravascular ultrasound study.

OBJECTIVE: To determine the impact of previous infection with cytomegalovirus, Chlamydia pneumoniae, and Helicobacter pylori on neointimal proliferation after coronary angioplasty with stent implantation. DESIGN: The study population was made up of 180 patients who had stent implantation in a native coronary artery with systematic angiographic and intravascular ultrasound (IVUS) follow up at six months. Quantitative coronary angiography was used to assess the late lumen loss. The mean area of neointimal tissue within the stent and the ratio of neointimal tissue to stent area were assessed from IVUS images. Previous cytomegalovirus, C pneumoniae, and H pylori infection was identified by IgG antibody determination. RESULTS: Previous cytomegalovirus infection was detected in 50% of the population, previous C pneumoniae in 18%, and previous H pylori in 33%. Mean (SD) reference diameter was 2.94 (0.48) mm and mean minimum lumen diameter after stent implantation was 2.45 (0.42) mm. At six months, the mean late loss was 0.74 (0.50) mm, the mean neointimal tissue area was 3.8 (1.7) mm(2), and the average ratio of neointimal tissue area to stent area was 45 (18)%. None of these variables of restenosis was linked to any of the three infectious agents. By multivariate analysis, lesion length was the variable best correlated with mean neointimal tissue area, the ratio of neointimal tissue to stent area, and late loss, explaining respectively 31%, 39%, and 8% of their variability. CONCLUSIONS: Previous infection with cytomegalovirus, C pneumoniae, or H pylori was not a contributing factor in the process of restenosis after stent implantation.

Left ventricular septal aneurysm in association with bicuspid aortic valve--a case report.

Diverticula of the left ventricle are rare cardiac anomalies. Most cases arise from the apex of the left ventricle and are usually found in children. Only a few cases have been documented in adults. The authors report a case of a 38-year-old woman who presented with dyspnea and chest pain. She was found to have a septal left ventricular diverticulum associated with bicuspid aortic valve, aortic stenosis, and aortic regurgitation. The aortic valve was replaced with the resection of the diverticulum. Pathologic examination confirmed the diagnosis of fibrous diverticulum.

A huge mitral valve tumor and its vascularity--a case report.

Primary cardiac tumors of the mitral valve are extremely rare; however, they present a major risk of embolization. Therefore, prompt diagnosis and urgent treatment is obligatory. The authors report the case of a 60-year-old man with a huge mitral valve mass and its vascularity, which was diagnosed by transthoracic echocardiography and selective coronary arteriography. Our patient's mitral valve tumor had a size of 5.9 x 2.9 cm, which was the largest size reported up to this time in this location. The patient died from a major cerebrovascular event before surgical excision could be performed.

T wave alternans can decrease after coronary revascularization.

Clinical observations and animal experiments indicate that T wave alternans (TWA) is associated with an increased propensity for ventricular fibrillation, and thus it may be considered as a noninvasive marker of life-threatening ventricular arrhythmias. There is substantial evidence indicating that TWA is an intrinsic property of ischemic myocardium. This study was performed to determine the role of percutaneous transluminal coronary angioplasty (PTCA)-induced myocardial ischemia in the development of TWA and the effects of revascularization. The authors recorded bipolar X, Y, and Z leads of 111 consecutive patients (mean age: 56 years) undergoing PTCA before, during, and 24 hours after the procedure. T wave alternans signal was calculated in 97 patients (43 left anterior descending, 26 right coronary artery, and 28 circumflex or major obtuse margin branch) by fast Fourier transformation technique after signal processing. Twenty-four hours after the procedure, the mean and peak X, Y, and Z values for TWA had all been significantly reduced from baseline and during balloon inflation (p<0.01). The findings point out that induced ischemia could be a trigger for T wave alternans, and successful revascularization can reduce alternans.

Is ventricular repolarization heterogeneity a cause of serious ventricular tachyarrhythmias in aortic valve stenosis?

BACKGROUND: It is well known that there is a close relation between sudden cardiac death and serious ventricular tachyarrhythmias in patients with aortic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repolarization heterogeneity and has been proposed as an indicator for ventricular arrhythmias. HYPOTHESIS: This study investigated the QTd and its relevance to the clinical and echocardiographic variables. METHODS: In all, 51 patients (33 men, 18 women, mean age 56 +/- 12) with isolated AS and 51 age- and gender-matched healthy controls comprised the study group. Left ventricular mass index (LVMI) was calculated by the Devereux formula, and we used continuous-wave Doppler (n = 15) and cardiac catheterization (n = 36) for the determination of the maximum aortic valve pressure gradient (PG). RESULTS: Corrected QTd (QTcd) (89 +/- 39 vs. 49 +/- 15 ms, p < 0.001) and LVMI (176 +/- 69 g/m2 vs. 101 +/- 28 g/m2, p < 0.001) in patients with AS were significantly different from those in the control group. The group of 21 patients had a significantly greater number of 24-h mean ventricular premature beats (VPB) and mean number of couplet VT episodes than did the control group (p < 0.05). QTcd also correlated significantly well with LVMI (r = 0.58, p < 0.001), PG (r = 0.41, p = 0.003), and number of 24-h VPB (r = 0.56, p = 0.008). With respect to symptoms (e.g., angina, syncope, and dyspnea) patients without symptoms (n = 19) displayed less QTcd (71 +/- 31 vs. 100 +/- 39 ms, p = 0.007) and less LVMI (144 +/- 80 g/m2 vs. 195 +/- 57 g/m2, p = 0.01) than patients with symptoms. Statistical analysis was similar for all variables with uncorrected QTd values. CONCLUSION: We found that ventricular repolarization heterogeneity was greater in patients with AS than in controls. Our findings also showed that QTd in the patient group correlates well with LVMI, severity of AS, and PG. The present results suggest that serious ventricular arrhythmias in patients with AS may be due to spatial ventricular repolarization abnormality.

Ruptured aneurysm of the sinus of Valsalva in association with persistent left superior vena cava--a case report.

A 58-year-old man presenting with chest pain and dyspnea was diagnosed by transesophageal echocardiography and cardiac catheterization to have the rare combination of ruptured aneurysm of noncoronary sinus of Valsalva into the right ventricle in association with persistent left superior vena cava. These defects were confirmed at cardiac surgery. This case shows the importance of complementary use of invasive and noninvasive methods together in the diagnosis of rare combinations of lesions.

Permanent left ventricular pacing from the great cardiac vein of a patient with artificial tricuspid and mitral valves--a case report.

Transvenous placement of a right ventricular pacemaker lead through the artificial tricuspid valve is a known contraindication, and in this situation, epicardial pacemaker implantation is the procedure of choice. However, permanent pacemaker implantation is a subject for debate when the use of the epicardial route is impossible. This report describes alternate transvenous routes for a pacemaker lead in a patient with an artificial tricuspid valve and mitral valve in whom the epicardial lead and pacemaker generator must be removed because of resistant infection.

Effects of stroke localization on cardiac autonomic balance and sudden death.

BACKGROUND AND PURPOSE: Stroke has been shown to alter autonomic function. The purpose of this study was to show the differential effects of stroke localization on autonomic function parameters assessed by heart rate variability (HRV). METHODS: To determine the differential effect of ischemic stroke localization on autonomic cardiac innervation, we evaluated 62 patients with ischemic stroke and 62 age- and sex-matched controls. The localization of the infarct was determined by CT and MRI. Power spectrum analysis of HRV was performed. Myocardial necrosis was ruled out by echocardiography and creatine kinase myocardial isoenzymes measurements. RESULTS: All stroke patients had significantly decreased low frequency, high frequency, and standard deviation of all relative risk intervals values (P<0.001). However, patients with right-middle cerebral artery (R-MCA) and insula lesions had significantly lower power spectrum analysis values compared with all other localizations (P<0.001). In addition, 5 patients with R-MCA insular lesions died suddenly compared with 2 patients with left-middle cerebral artery insular lesions during hospitalization. Both sympathetic- and parasympathetic-controlled HRV were decreased in patients with ischemic stroke. The most pronounced decrease was found in the territory of R-MCA insular cortex, which suggests that cardiac autonomic tone may be regulated by insula and that these patients are more prone to cardiac complications such as arrhythmias and sudden death due to autonomic imbalance. CONCLUSION: We conclude that stroke in the region of insula (especially the right) leads to decreased HRV and to increased incidence of sudden death.

Circadian variations of QTc dispersion: is it a clue to morning increase of sudden cardiac death?

BACKGROUND: Several studies related to cardiac events including sudden death have shown a peak incidence in the early morning hours. It has also been known that acute ischemia is a potent stimulus to increased dispersion of repolarization and development of malignant arrhythmias. HYPOTHESIS: The purpose of the present study was to investigate diurnal variations of corrected QT dispersion (QTcD) in patients with coronary artery disease (CAD) (Group 1) compared with controls with normal coronary angiograms (Group 2). METHODS: We investigated a total of 110 patients who had been referred for coronary angiography, of whom 62 (42 men, 20 women; age 55 +/- 7 years) had double- or triple-vessel disease, and of whom 48 (31 men, 17 women; age 54 +/- 9 years) had normal coronary angiograms. QTcD measurements were calculated from a 12-lead resting electrocardiogram (ECG) during sinus rhythm. These ECGs were obtained for each patient in the morning, at noon, in the evening, and at night on the day after performance of coronary angiography. QTcD was significantly greater in patients with abnormal coronary angiograms (Group 1) than in patients with angiographically documented normal coronary arteries (Group 2). This difference appeared to be more prominent in the morning hours (p < 0.001) than at other times. QTcD in the evening and night hours was not statistically different (p > 0.05) between both groups. We also compared intragroup QTcD values: QTcD values were significantly increased in the morning hours and were more prominent in Group 1 than in Group 2. CONCLUSIONS: Our data suggest that QTcD has a circadian variation with an increase in the morning hours, especially in patients with coronary artery disease. This finding was thought to be an explanation for the role played by sympathetic nervous system in the occurrence of acute cardiac events and sudden death during these hours.

Thrombosis involving the major veins with heterozygote factor V Leiden mutation as the only risk factor.

A 27-year-old man was admitted to our hospital with the complaints of swelling of his face and lower limbs. Echocardiography showed minimal pericardial effusion accompanied by disordered diastolic function. Cardiac catheterization was performed to rule out constrictive pericarditis. Normal pressure tracings of the right heart rule out constrictive pericarditis, however, a narrowing of the inferior vena cava was observed. Venographies of the inferior and superior vena cavae showed extensive thrombotic involvement of these great veins. Protein C, protein S, anticardiolipin antibodies, fibrinogen, antithrombin-III, activated protein C resistance, and factor V levels were in normal limits. Heterozygosity for factor V Leiden mutation was detected. We conclude that factor V Leiden mutation can cause extensive thrombotic involvement of major veins and should be considered in idiopathic thrombosis of them.

Comparison of the three different formulas for Doppler estimation of pulmonary artery systolic pressure.

Noninvasive pulmonary artery systolic pressure (PASP) is calculated by summing the right ventricular systolic pressure obtained from Doppler velocity of regurgitant flow through the tricuspid valve and the right atrial (RA) pressure. The RA pressure is generally assumed from different formulas. An accurate RA pressure estimation will add precision to PASP calculation. One of the methods to estimate RA pressure is the inferior vena cava collapsibility index (IVCCI). In 45 patients referred for right heart catheterization, the authors tested a formula for the calculation of PASP based on the estimation of RA pressure from IVCCI and compared this method with two other formulas. The first method (method 1) assumed a constant RA pressure of 10 mm Hg irrespective of right ventricular pressure. The formula used was Doppler gradient + 10 (mm Hg). In the second method (method 2), a clinical estimate of RV pressure was made from the formula: right ventricular-right atrial Doppler gradient x 1.1 + 14. In the third method (method 3), the patients were classified into three groups on the basis of IVCCI: group A, IVCCI greater than 45%; group B, IVCCI between 35% and 45%; and group C, IVCCI less than 35%. The formula used was Doppler gradient + 6, 9, or 16 mm Hg in the presence of normal (group A), moderately reduced (group B), or markedly reduced (group 3) IVCCI. A good correlation between Doppler and catheter measurements of PASP was found for methods 1, 2, and 3, respectively (r=0.8933, SEE=6.4, r=0.8921, SEE=7.0, and r=0.8989, SEE=6.7). Correlation between invasive and noninvasive PASP was similar with the three methods, but correlation in method 2 was less satisfactory than with the other two methods. The mean difference between Doppler-derived and hemodynamic PASP was also high in method 2. In conclusion, the result of this study validates a relatively new, simple echo-Doppler formula for Doppler estimation of PASP based on a noninvasive evaluation of RA pressure through the IVCCI. However, this method is not better than the traditional method 1 for noninvasive PASP estimation.