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 (PϽ0.001). However, patients with right-middle cerebral artery (R-MCA) and insula lesions had significantly lower power spectrum analysis values compared with all other localizations (PϽ0.001). 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.
The present study has been designed to determine melatonin levels in type 2 diabetic patients and test the relationship between the autonomic nervous system and melatonin dynamics. Thirty-six type 2 diabetic patients and 13 age-matched healthy subjects were recruited for the study. Circadian rhythm of melatonin secretion was assessed by measuring serum melatonin concentrations between 02:00-04:00 and 16:00-18:00 hr. Melatonin dynamics were re-evaluated with respect to autonomic nervous system in diabetic patients with autonomic neuropathy who were diagnosed by the cardiovascular reflex tests, heart rate variability (HRV), and 24-hr blood pressure monitoring. Nocturnal melatonin levels and the nocturnal melatonin surge were low in the diabetic group (P = 0.027 and 0.008 respectively). Patients with autonomic neuropathy revealed decreased melatonin levels both at night and during day when compared with healthy controls (P < 0.001 and 0.004 respectively) while the melatonin dynamics were similar to controls in patients without autonomic neuropathy. Nocturnal melatonin level was positively correlated with nocturnal high and low frequency components of HRV (P = 0.005 and 0.011 respectively) and systolic and diastolic blood pressures at night (P = 0.002 and 0.004 respectively) in patients with autonomic neuropathy. We found a negative correlation between nocturnal melatonin levels and the degree of systolic blood pressure decrease at night (r = -0.478, P = 0.045). As a conclusion this study has shown that circadian rhythm of melatonin secretion is blunted in type 2 diabetic patients and there is a complex relationship between various components of autonomic nervous system and melatonin secretion at night. Among the patients with autonomic neuropathy those with more preserved HRV and the systolic nondippers (<10% reduction in blood pressure during the night relative to daytime values) have more pronounced melatonin surge at night.
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.
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.
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.
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