Different humoral responses during head-up tilt testing among patients with neurocardiogenic syncope.

Neurocardiogenic dysfunction is believed to result from activation of ventricular mechanoreceptors. To asses other humoral and circulatory mechanisms activated during vasovagal syncope, epinephrine, norepinephrine, renin, and aldosterone levels were measured during head-up tilt testing. Twenty-three patients referred because of vasovagal syncope underwent passive head-up tilt testing (80 degrees). Blood samples were taken at baseline, after 30 minutes of supine rest and at syncope. Five patients (four men, one woman; mean age 46 +/- 27 years) had cardioinhibitory syncope. Seven patients (five men, two women; mean age 40 +/- 12 years) had vasodepressor syncope. Eleven patients (eight men, three women; mean age 55 +/- 21 years) had negative results of head-up tilt tests. Among patients with cardioinhibitory syncope, norepinephrine concentration rose significantly from baseline to syncope (0.44 +/- 0.12 ng/ml versus 1.14 +/- 0.72 ng/ml; p < 0.05), whereas no significant change was observed in epinephrine (0.08 +/- 0.03 ng/ml versus 2.74 +/- 2.85 ng/ml; p = not significant [NS]), renin (5.68 +/- 3.03 pg/ml versus 19.58 +/- 11.47 pg/ml; p = NS), or aldosterone concentration (66.60 +/- 16.10 ng/ml versus 109.00 +/- 44.70 ng/ml; p = NS). Patients with vasodepressor syncope had a significant rise in renin (9.03 +/- 4.56 pg/ml versus 52.53 +/- 41.63 pg/ml; p < 0.05) and aldosterone concentration (95.43 +/- 103.03 ng/ml versus 249.57 +/- 191.54 ng/ml; p < 0.05), whereas no change in level of epinephrine (0.12 +/- 0.12 ng/ml versus 0.28 +/- 0.33 ng/ml; p = NS) or norepinephrine (0.60 +/- 0.26 ng/ml versus 0.86 +/- 0.53 ng/ml; p = NS) was detected. Among patients with negative results of tilt tests, levels of renin (7.94 +/- 7.19 pg/ml versus 27.71 +/- 18.50 pg/ml; p < 0.01) and aldosterone (64.64 +/- 28.33 ng/ml versus 160.91 +/- 79.58 ng/ml; p < 0.01) rose significantly, whereas no change was seen in epinephrine (0.12 +/- 0.14 ng/ml versus 0.23 +/- 0.31; p = NS) or norepinephrine concentration (0.54 +/- 0.21 ng/ml versus 0.82 +/- 0.52; p = NS). Patients with cardioinhibitory syncope were characterized by a rise in norepinephrine level and blunted activation of the renin-angiotensin-aldosterone axis at syncope. Unlike patients with cardioinhibitory syncope, the renin-angiotensin-aldosterone axis is activated in patients with vasodepressor syncope and patients with a negative result of head-up tilt test without a statistically significant increase in catecholamine levels. Patients with cardioinhibitory syncope have higher epinephrine levels at syncope compared with patients with a negative result of head-up tilt test and patients with vasodepressor syncope.

Pacing induced mitral regurgitation following radiofrequency ablation of the atrioventricular conduction system: case report and potential mechanism.

We describe a patient with hemodynamic deterioration and worsening mitral regurgitation related to right ventricular apex pacing. Time-dependent changes in papillary muscle contraction as well as ventricular remodeling by right ventricular apex pacing might be responsible for this rare but serious complication.

Hemodynamic deterioration following radiofrequency ablation of the atrioventricular conduction system.

Radiofrequency ablation of the atrioventricular conduction system (ACS) has become an established therapy for patients with drug refractory atrial fibrillation. We observed eight patients with hemodynamic deterioration after radiofrequency ablation of the atrioventricular conduction system. As we found hemodynamic deterioration related to worsening mitral regurgitation, we compared the clinical history, electrophysiological, and echocardiographic data from the patients with hemodynamic deterioration and worsening mitral regurgitation (group 1) to those without hemodynamic deterioration and stable mitral regurgitation after the procedure (group 2). Eight out of 108 patients (7.4%) undergoing ablation of the ACS deteriorated hemodynamically with acute pulmonary edema in three and congestive heart failure in five patients occurring at a mean of 3 and 8 weeks, respectively, after the procedure. Three of these patients were referred for mitral valve surgery. Two patients underwent ablation using a left-sided approach. A right-sided approach was used in five patients. In one patient, a left- and right-sided approach was used. Compared to group 2 patients, group 1 patients had significantly higher left ventricular end-diastolic diameters (64 +/- 6 mm vs 56 +/- 9 mm) at baseline despite similar fractional shortening (32% +/- 11% vs 34% +/- 13%), left ventricular end-systolic diameters (43 +/- 9 mm vs 36 +/- 7 mm) and degree of mitral regurgitation (1.4 +/- 1.1 vs 1.4 +/- 0.7) on echocardiographic analysis. Thus, hemodynamic deterioration together with progression of mitral regurgitation is a potential complication of ablation of the ACS (up to 7.4%). Patients with high left ventricular end-diastolic diameters and moderate mitral regurgitation at baseline seem prone to this complication.

Herniation of the left atrial appendage due to partial congenital absence of the left pericardium.

Partial congenital absence of the left pericardium is a rare abnormality which may provoke serious complications. We report the case of a young adult, suffering from chest pain due to incarceration of atrial tissue. Based on this case report the clinical, pathophysiological and diagnostic features of this condition are described.

Catheter ablation of ventricular tachycardia occurring late after myocardial infarction: a point-of-view.

Ventricular tachycardia can be controlled by radiofrequency or chemical ablation of the site of origin of the arrhythmia. However, these techniques are far from being accepted as routine treatment for this problem. This article describes the theoretical and practical background of catheter ablation of ventricular tachycardia occurring late after myocardial infarction.

Epicardial and subselective transcoronary chemical ablation of incessant ventricular tachycardia.

Incessant ventricular tachycardia in patients with severely depressed ventricular function remains a major therapeutic challenge. Although alcohol ablation via the tachycardia related vessel has been shown to be an effective alternative, it might not be applicable in some cases due to anatomic limitations. In three patients with ischemic cardiomyopathy and incessant ventricular tachycardia no effective antiarrhythmic therapy could be found. Alcohol ablation was then attempted but the tachycardia related vessel could not be intubated. A subselective injection of alcohol into a more proximal segment of the coronary artery was then performed in two cases. In one patient as subselective injection was also not possible, the injection was performed epicardially after thoracotomy. Ablation was successful in all cases. In very selected cases of incessant ventricular tachycardia that have failed all other therapeutic interventions, alcohol ablation of the tachycardia can be performed using an epicardial or subselective transcoronary injection of alcohol.

Transcoronary chemical ablation of arrhythmias.

BACKGROUND: Chemical or electrical ablation of an arrhythmogenic ventricular area and the atrioventricular (AV) node is still an experimental technique. After we introduced alcohol ablation in the clinical situation we conducted this study to develop the catheter technique for delivering alcohol in patients with incessant ventricular tachycardia after myocardial infarction and patients with atrial fibrillation and flutter with uncontrollable ventricular rates. METHODS: In patients with incessant ventricular tachycardia, the coronary artery supplying blood to the site of origin of the tachycardia could be identified by the combined information from coronary and left ventricular angiography and from programmed electrical stimulation, including endocardial mapping and pace mapping. In the 12 patients with incessant ventricular tachycardia we selected, the coronary artery supplying blood to the site of origin of the tachycardia could be identified and catheterized in ten patients. Ethanol ablation was successful in all of them. With a follow-up from 2 to 44 months, seven of the ten treated patients are still alive and six remain free of tachycardia. In patients with atrial fibrillation or flutter and uncontrollable ventricular rates, the AV artery could be catheterized and ethanol injected in 13 of the 19 patients. Complete block was produced in ten patients and AV conduction was sufficiently modified to control symptoms in three patients. Long-term results with ethanol ablation have remained excellent in this setting. CONCLUSION: Chemical ablation is a technique that may be of enormous value and even lifesaving for patients with an incessant form of tachycardia not responding to any form of medical therapy. Transcoronary ablation of AV conduction should be considered in patients with a right dominant coronary circulation in whom radiofrequency ablation has failed.

Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy.

Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 +/- 17 to 74 +/- 21 msec (p less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation.

Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy.

The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.

Internal mammary to pulmonary artery fistula associated with healed tuberculosis.

An internal mammary to pulmonary artery fistula was diagnosed in a patient with a continuous machinery-like murmur over the right upper chest wall 23 years after she was treated for pulmonary tuberculosis.

Depression of regional blood flow and wall thickening after brief coronary occlusions.

The effects of a 15-min coronary occlusion and subsequent reperfusion were investigated in conscious dogs previously instrumented for measurement of left ventricular pressure, dP/dt, regional wall thickening, electrograms, and myocardial blood flow. Coronary occlussion reduced overall left ventricular function only slightly but eliminated systolic wall thickening in the ischemic zone and reduced regional myocardial blood flow in the ischemic zone from 1.04 +/- 0.04 to 0.27 +/- 0.02 ml/min per g and the endo/epi flow ratio from 1.23 +/- 0.04 to 0.44 +/- 0.04, while S-T segment elevation increased from 1.1 +/- 0.3 to 8.2 +/- 0.9 mV. After release of the occlusion, S-T segment elevation disappeared within 1 min while reactive hyperemia in the previously occluded artery and a transient increase in cardiac diastolic wall thickness occurred and then subsided by 15 min. In contrast, systolic wall thickening and the endo/epi flow ratio remained significantly depressed for more than 3 h. Thus reperfusion after a 15 minute coronary occlusion results in a prolonged period of reduced regional myocardial blood flow, particularly in the endocardial layers, which correlates with the prolonged depression of regional myocardial shortening and wall thickening.