Biochemical changes involved in the mechanism of vasovagal syncope.

Vasovagal syncope elicits one of the most powerful transient vasodilatory responses in humans. Many studies have shown an altered neurohumoral response to tilting in patients with vasovagal syncope. Vasopressin (VP) has been of particular interest, but its exact role remains unclarified, whereas the possible role of the potent vasoactive end products of arachidonic acid metabolism has not yet been addressed. We determined the changes in plasma levels of VP, thromboxane (TXA2), and prostacyclin (PGI2) in 34 syncopal patients undergoing a standardized head-up tilt-table testing protocol and compared these changes between patients with positive and negative test results. Blood samples were collected at baseline, 15 minutes in the head-up position, and at the termination of the tilt test (the induction of syncope or the completion of a negative test). Sixteen patients had a positive test result, whereas 18 completed the test without developing any syncopal symptoms. In the tilt-positive group, VP levels presented a 20-fold increase at the time of syncope when compared with baseline levels (p = 0.0000), without any increase at earlier stages. No change was detected at any stage in the tilt-negative patients. We did not find any difference in the levels of PGI2 at any stage in any group of patients or between the 2 groups. TXA2 levels increased significantly at 15 minutes in the upright position in both tilt-positive and tilt-negative patients. No further increase was noticed at the time of syncope in the tilt-positive group, whereas in patients with a negative test result, there was a tendency to decline at the time of the test's completion. It is concluded that although VP is markedly increased during tilt-induced vasovagal syncope, vasoactive amines such as TXA2 and PGI2 play a minor role in the vasodilatory component of the response.

Electromyographic evidence of subclinical myopathy in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is due to a number of mutations of contractile protein genes such as beta-cardiac myosin, myosin binding protein-C, and troponin-T. Unlike troponin-T, beta-myosin is a constituent of slow skeletal muscle and its mutations generally have a better prognosis. In order to investigate the usefulness of electromyography in detecting skeletal muscle involvement in HCM, 46 patients were examined using both conventional electromyography (EMG) and quantitative electromyography (QEMG) methods. The QEMG involved motor unit potential (MUP) analysis, turns/amplitude (TAA) analysis, and power spectrum analysis of the interference pattern. Using conventional EMG, myopathic findings were demonstrated in 13 patients (28%). Receiver operating characteristic (ROC) analysis of the results of a discriminant function extracted using QEMG values, identified correctly 10 out of 11 normal controls and all 9 myopathic control patients, and displayed a 15% presence of myopathy (7 patients) among the cardiomyopathy group. The duration of MUPs was the most sensitive among the quantitative parameters in differentiating normal from myopathic subjects. Since skeletal muscle involvement may be due to distinct gene mutations, normal and myopathic EMG findings may reflect HCM subpopulations with a different genetic substrate.

Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 +/- 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.

Cardiomyopathy due to a pheochromocytoma. A reversible entity.

A 45-year-old male presented with acute pulmonary oedema, chest pain and electrocardiographic manifestations of acute myocardial ischaemia in the setting of hypertension crisis from a hyperfunctioning large left-sided pheochromocytoma. Coronary artery disease was excluded on the basis of thallium stress testing and coronary angiography. The latter revealed a picture consistent with dilated cardiomyopathy. After surgical resection of the tumour, both the hypercatecholaminaemia and the arterial hypertension subsided promptly with gradual improvement of the cardiomyopathy and complete resolution of the congestive heart failure symptoms.

Hypertrophic cardiomyopathy in Greece: clinical course and outcome.

OBJECTIVE: Evaluation of clinical course and outcome of hypertrophic cardiomyopathy in a representative Greek population. BACKGROUND: Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy and varied clinical expression. Recent studies suggest ethnic differences. MATERIALS AND METHODS: One hundred seventy-four consecutive Greek patients (117 male, 57 female, age 47+/-16 years) from 143 different families were assessed at the Department of Cardiology of the University of Athens, Greece, and the State Cardiac Department, Hippokration Hospital, both located in Athens, Greece. To reduce selection bias, referral was based on disease diagnosis irrespective of clinical status or treatment needs. All patients were examined clinically, echocardiographically, and by ECG ambulatory monitoring at 6-month intervals for a period of 74+/-22 months (range, 8 to 108 months). RESULTS: Most patients (n = 156, 89.7%) were in New York Heart Association (NYHA) functional class I or II. The disease was familial (at least one affected first-degree relative) in 81 of the 143 families (56.6%), and in 19 of these (13.3%) there was familial history of sudden cardiac death. At initial examination, intraventricular septal thickness was 17.3+/-4.1 mm and posterior wall thickness was 13.7+/-3.8 mm and a left ventricular outflow gradient >30 mm Hg was present in 58 patients (33.3%). Similar were the findings during the last examination (17.5+/-4.3 mm, 13.5+/-4.4 mm, and 56 (32.2%, respectively, p = not significant). Episodes of nonsustained ventricular tachycardia were noted in 15 patients (8.6%). There were eight deaths during follow-up: four sudden deaths and four from intractable heart failure. Syncope was reported by all patients who died. The annual mortality in this study was 1%. Syncope and NYHA class were the only predictors of outcome. CONCLUSIONS: In this representative Greek patient cohort with hypertrophic cardiomyopathy, the arrhythmogenic substrate was modest and the clinical course benign. Sudden cardiac death was infrequent and syncope, functional class, and ventricular arrhythmias were the only predictors of a poor outcome.

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.

Usefulness of noninvasive detection of left ventricular diastolic abnormalities during isometric stress in hypertrophic cardiomyopathy and in athletes.

We showed previously that the handgrip apexcardiographic test (HAT) is a useful method for detecting left ventricular (LV) diastolic abnormalities in patients with coronary artery disease and systemic hypertension. This study evaluates the use of HAT for assessing the prevalence and types of exercise-induced diastolic abnormalities in patients with obstructive (n = 31) and nonobstructive (n = 35) hypertrophic cardiomyopathy (HC) as well as its potential value for separating healthy subjects and athletes from patients with HC. We obtained a HAT in 66 consecutive patients with HC and in 72 controls (52 healthy volunteers and 20 athletes). A positive HAT was defined by the presence of one of the following: (1) relative A wave to total height (A/H) during or after handgrip > 21% (compliance type), (2) total apexcardiographic relaxation time (TART) > 143 ms or the heart rate corrected TART (TARTI) during handgrip < 0.14, (relaxation type), (3) both types present (mixed type), and (4) diastolic amplitude time index (DATI = TARTI/[A/D]) during handgrip < 0.27. Of the controls, only 1 of 52 healthy subjects and 1 of 20 athletes showed a positive HAT, whereas of the total HC cohort 63 of 66 patients (95%) had a positive result. There was no significant difference in the distribution of these types between obstructive and nonobstructive HC. Further, no LV diastolic abnormalities were present in 10 of 35 patients (29%) with nonobstructive HC at rest and in 3 of 35 patients (9%) during handgrip, whereas of the patients with obstructive HC only 1 of 31 (3%) had no LV diastolic abnormalities at rest and none during handgrip. Based on HAT data, our study demonstrates that in HC (1) LV diastolic abnormalities are very frequent during handgrip; (2) patients with nonobstructive HC show significantly fewer LV diastolic abnormalities at rest than those with obstructive HC; and (3) no significant difference exists between obstructive and nonobstructive HC in the prevalence of types of handgrip-induced LV diastolic abnormalities. Consequently, HAT appears to be of clinical value as an additional tool for separating normal patients and athletes from patients with HC.