Ioannis P. Panidis

Sudden death in hospitalized patients: cardiac rhythm disturbances detected by ambulatory electrocardiographic monitoring.

To determine the cardiac rhythm disturbances underlying sudden death, 15 patients (14 inpatients and 1 outpatient) who had cardiac arrest unexpectedly while undergoing ambulatory electrocardiographic monitoring were identified. Heart disease was present in 11 patients and 7 patients were admitted to the hospital with chest pain before sudden cardiac death occurred. The terminal event at the time of cardiac arrest in 3 (20%) of the 15 patients was a bradyarrhythmia expressed as complete heart block; none survived. A ventricular tachyarrhythmia was the precursor of sudden cardiac death in the remaining 12 patients (80%). Two of these 12 had slow ventricular tachycardia and both died. Five had polymorphous ventricular tachycardia associated with prolonged QT interval (torsade de pointes) and three were receiving a class I antiarrhythmic agent. This rhythm degenerated into ventricular fibrillation in one patient; four of the five patients survived after electrical cardioversion. One patient had ventricular tachycardia followed by asystole. Four patients had ventricular flutter (rate greater than 250/min) that degenerated into ventricular fibrillation in each case; only one of these four patients survived after cardioversion. Frequent (greater than 30/h) premature ventricular complexes were present in 9 of 10 patients with ventricular tachycardia or flutter and R on T phenomenon was seen in only 1 patient. In conclusion, a ventricular tachyarrhythmia is usually found on Holter monitoring during sudden cardiac death in hospitalized patients; torsade de pointes (polymorphous ventricular tachycardia) is a frequent cause of sudden death in these patients. Ventricular fibrillation is always preceded by ventricular tachycardia or ventricular flutter.

Normal and abnormal prosthetic valve function as assessed by doppler echocardiography

Doppler echocardiography was performed in 136 patients with a normally functioning prosthetic valve in the aortic (n = 59), mitral (n = 74) and tricuspid (n = 3) positions. These included patients with St. Jude (n = 82), Björk-Shiley (n = 18), Beall (n = 13), Starr-Edwards (n = 7) or tissue (n = 16) valves. Peak and mean pressure gradients across the prostheses were measured using the simplified Bernoulli equation. The prosthetic valve orifice (PVO, in square centimeters), only in the mitral position, was calculated by the equation: PVO = 220/pressure half-time. In the aortic position, the St. Jude valve had a lower peak velocity (2.3 +/- 0.6 m/s, range 1.0 to 3.9), peak gradient (22 +/- 12 mm Hg, range 4 to 61) and mean gradient (12 +/- 7 mm Hg, range 2 to 32) than the other valves (p less than 0.05) when compared with Starr-Edwards). In the mitral position, the St. Jude valve had the largest orifice (3.0 +/- 0.6 cm2, range 1.8 to 5.0) (p less than 0.0001 compared with all other valves). Insignificant regurgitation was commonly found by pulsed mode Doppler technique in patients with a St. Jude or Björk-Shiley valve in the aortic or mitral position and in patients with a Starr-Edwards or tissue valve in the aortic position. In 17 other patients with a malfunctioning prosthesis (four St. Jude, two Björk-Shiley, four Beall and seven tissue valves) proven by cardiac catheterization, surgery or autopsy, Doppler echocardiography correctly identified the complication (significant regurgitation or obstruction) in all but 2 patients who had a Beall valve. It is concluded that 1) the St. Jude valve appears to have the most optimal hemodynamics; mild regurgitation can be detected by the Doppler technique in normally functioning St. Jude and Björk-Shiley valves in the aortic or mitral position and in Starr-Edwards and tissue valves in the aortic position, and 2) Doppler echocardiography is a useful method for the detection of prosthetic valve malfunction, especially when the St. Jude, Björk-Shiley and tissue valves are assessed.

Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by doppler echocardiography

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Wenckebach type) and 3 patients with third degree AV block; 20 individuals with a normal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to mitral valve closure interval measured 220 +/- 30 ms by M-mode and to the end of mitral flow 225 +/- 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 +/- 41 and 249 +/- 36 ms, respectively (p = NS). Late diastolic (before the onset of the QRS complex) mitral regurgitation was detected by pulsed mode Doppler imaging in 9 (56%) of the 16 patients with first degree AV block but in none with a normal PR interval. In the four patients with advanced AV block, intermittent mid or late diastolic mitral regurgitation was found to depend on the position of the P wave in diastole. With early diastolic P waves, the end of mitral valve flow by Doppler technique occurred 230 to 250 ms after the onset of the P wave and was followed by mild diastolic mitral regurgitation of variable duration. With P waves falling in systole, the mitral valve remained open throughout diastole; during most of diastole, however, there was neither forward mitral flow (diastasis) nor diastolic mitral regurgitation detected by Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of octreotide in patients with autonomic neuropathy.

BackgroundThe somatostatin analogue, octreotide, is being used to treat postprandial hypotension in patients with autonomic neuropathy. Although the therapeutic effect of the drug is presumably secondary to a splanchnic vasoconstrictor action, its effect on splanchnic hemodynamics has never been characterized in patients with autonomic neuropathy. Moreover, is unknown whether octreotide acts on other vascular beds in this group of patients or whether it affects cardiac output. We, therefore, measured splanchnic, forearm, and systemic vascular resistance and cardiac output before and after administering octreotide (0.4 μg/kg s.c.) to patients with idiopathic autonomic neuropathy and diabetic autonomic neuropathy. Methods and ResultsSplanchnic blood flow was determined from the clearance of indocyanine green in seven patients. We observed that octreotide decreased splanchnic blood flow (from 850±77 to 664±48 ml/min, p < 0.005), increased mean blood pressure (from 97±6 to 115±3 mm Hg, p < 0.005), and increased splanchnic vascular resistance (from 0.118±0.012 to 0.18 ±0.018 mm Hg/ml/min, p < 00.005). Forearm blood flow was measured by plethysmography in 13 patients. Octreotide increased forearm vascular resistance in patients with idiopathic autonomic neuropathy (n =8) from 19.1 ± 1.0 to 27.2±3.8 mm Hg/ml/min/100 ml forearm volume (p < 0.01) and from 25.2±3.9 to 41.0±6.8 mm Hg/ml/min/100 ml (p < 0.01) in patients with diabetic autonomic neuropathy (n =5). Cardiac output was measured by two-dimensional echocardiography. Octreotide administration increased cardiac output in five of six patients with idiopathic autonomic neuropathy (from 4.4 0.4 to 5.0 ± 0.5 1/min, p < 0.02) and five of five patients with diabetic autonomic neuropathy (from 3.8 ± 0.4 to 5.1 ± 0.4 1/min, p < 0.02). Systemic vascular resistance increased in patients with idiopathic autonomic neuropathy from 21.2±2 to 24.9±2.6 (p < 0.05) but did not change in patients with diabetic autonomic neuropathy. ConclusionsThe pressor effect of octreotide in patients with autonomic neuropathy is associated with increased splanchnic and forearm vascular resistance and with increased cardiac output. (Circulation 1991;84:168–176)

Noninvasive evaluation of normal and abnormal prosthetic valve function.

Noninvasive techniques are helpful in evaluating the function of mechanical prostheses and tissue valves. Combined phonocardiography and M-mode echocardiography together with cinefluoroscopy are the most useful noninvasive techniques in differentiating normal from abnormal metallic prosthetic valve function. The intensity of the opening and closing clicks and associated murmurs will depend on the type of prosthetic valve, the heart rate and rhythm and the underlying hemodynamic status. Arrhythmias or conduction disturbances, or both, may produce motion patterns that mimic some of the echocardiographic signs of malfunctioning prosthetic valves. Differentiation of thrombus formation or tissue ingrowth from paravalvular regurgitation or dehiscence is possible by noninvasive techniques. Disc variance, a potentially serious and lethal problem with the older Beall valves, can be readily detected by cinefluoroscopy and echophonocardiography. With regard to bioprosthetic valves, two-dimensional echocardiography is superior to M-mode echocardiography in detecting primary valve failure. In addition, detection of vegetations, valve alignment and ring and individual leaflet motion can be best accomplished by two-dimensional echocardiography. Of greater importance is the patient serving as his or her own control in the follow-up assessment of prosthetic valve function by noninvasive techniques.

Two-dimensional echocardiographic estimation of right ventricular ejection fraction in patients with coronary artery disease

Two-dimensional echocardiographic determination of right ventricular ejection fraction was compared with right ventricular ejection fraction obtained by first pass radionuclide angiography in 39 patients with coronary artery disease. Apical four chamber and two chamber right ventricular views were obtained in 34 (87%) of the 39 patients, while a subcostal four chamber view was obtained in 31 patients (80%). Right ventricular ejection fraction by two-dimensional echocardiography was calculated by the biplane area-length and Simpsons rule methods using two paired orthogonal views and utilizing a computerized light-pen method for tracing the right ventricular endocardium. A good correlation (r = 0.74 to 0.78) was found between radionuclide angiographic and two-dimensional echocardiographic right ventricular ejection fraction for each method used. Patients with acute inferior myocardial infarction had the lowest right ventricular ejection fraction by radionuclide angiography and two-dimensional echocardiography (p less than 0.05 compared with patients with right coronary artery obstruction and no infarction). There were no differences in right ventricular ejection fraction between patients with acute and old inferior myocardial infarction by both techniques. No correlation was found between left and right ventricular ejection fraction by radionuclide angiography (r = 0.16). It is concluded that 1) right ventricular ejection fraction by two-dimensional echocardiography correlates well with radionuclide angiographic measurements and can reliably evaluate right ventricular function in coronary artery disease, 2) patients with inferior myocardial infarction have reduced right ventricular ejection fraction, and 3) changes in left ventricular ejection fraction do not directly influence right ventricular function.

The value of echocardiographic regional wall motion abnormalities in detecting coronary artery disease in patients with or without a dilated left ventricle

To evaluate the usefulness of echocardiographic regional wall motion abnormalities (RWMA) in detecting coronary artery disease (CAD) in patients with left ventricular (LV) dysfunction and a normal-sized or dilated left ventricle, 103 patients were studied by two-dimensional echocardiography (2DE) and cardiac catheterization. In 60 patients (group I) who had LV dysfunction and a dilated left ventricle by echo (patients with dilated cardiomyopathy), RWMA were detected in 44 patients and 38 (86%) of them had significant CAD, usually two- or three-vessel obstruction; of the 16 patients with dilated cardiomyopathy (DCM) and diffuse LV hypokinesis, eight (50%) had evidence of CAD. Thus the presence of RWMA by 2DE had an 83% sensitivity, a 57% specificity, and a 77% predictive accuracy in detecting CAD in patients with DCM and thus in distinguishing ischemic from idiopathic DCM. In 43 patients with LV dysfunction but normal LV size (group II), the sensitivity, specificity, and predictive accuracy of RWMA in detecting significant CAD was 95%, 100%, and 95%, respectively. We conclude that the detection of RWMA by 2DE is highly suggestive of significant CAD in patients with LV dysfunction and normal-sized or dilated left ventricle; the finding, however, of diffuse LV hypokinesis does not exclude CAD in these patients, especially when the left ventricle is dilated.

Effects of esmolol on patients with left ventricular dysfunction

This study examined the effect of esmolol, an ultrashort-acting beta-receptor blocker, in 10 patients with severe left ventricular dysfunction. Simultaneous hemodynamic and radionuclide angiographic measurements were obtained at incremental doses of esmolol (2, 4, 8, 12 and 16 mg/min). At a dose of 4 mg/min, esmolol produced beats blockade: a decrease in heart rate from 91 +/- 4 to 83 +/- 4 beats/min (p less than 0.05) (mean +/- SEM) and a decrease in systolic aortic pressure from 133 +/- 5 to 128 +/- 5 mm Hg (p less than 0.05). At the maximal dose, the heart rate decreased to 79 +/- 3 beats/min (p less than 0.05) and biventricular function was depressed; the left ventricular ejection fraction decreased from 27 +/- 2 to 21 +/- 2% (p less than 0.05) and the right ventricular ejection fraction decreased from 38 +/- 2 to 29 +/- 2% (p less than 0.05). These changes were accompanied by increases in left ventricular end-diastolic volume (p less than 0.05), left ventricular end-systolic volume (p less than 0.05) and pulmonary artery wedge pressure (p less than 0.05), as well as a decrease in cardiac output (p less than 0.05). The hemodynamic abnormalities (which showed considerable interindividual variability) returned to near baseline levels 10 to 30 minutes after infusion was stopped. Thus, esmolol can be administered to patients with severe left ventricular dysfunction. The beneficial effect (beta-adrenergic blockade) is usually achieved with small doses without clinically important hemodynamic changes. At larger doses, however, significant changes in biventricular function may be observed.

Prevalence and severity of mitral regurgitation in the mitral valve prolapse syndrome: a Doppler echocardiographic study of 80 patients

Doppler echocardiography was performed in 80 consecutive patients (22 men, 58 women), aged 38 +/- 16 years, who had mitral valve prolapse diagnosed by two-dimensional echocardiography. Of the 80 patients, 16 (20%) were asymptomatic and 11 (14%) had a normal physical examination (no click or murmur). The M-mode echocardiogram was negative for mitral valve prolapse in 11 patients (14%) and equivocal or nondiagnostic in 19 patients (24%). Mitral regurgitation was evaluated using pulsed mode Doppler echocardiography and was quantified by the mapping technique as minimal or mild when a holosystolic regurgitant jet was recorded just below the mitral valve into the left atrium, and as moderate or severe when the jet was detected at the mid- or distal left atrium. Mitral regurgitation was found in 55 (69%) of the 80 patients and it was minimal or mild in 47 patients (59%) and moderate or severe in 8 (10%). In 20 (36%) of the 55 patients with mitral regurgitation by Doppler technique, a systolic murmur was not detected and each of the 20 had only mild mitral regurgitation. Left atrial and left ventricular size were significantly smaller in patients with mild or no regurgitation as compared with the eight patients with moderate or severe regurgitation. These eight patients were all men (six over 50 years of age) who usually presented with dyspnea and a holosystolic murmur; the mitral valve prolapse was holosystolic by M-mode and involved both leaflets by two-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Effectiveness and safety of oral verapamil to control exercise-induced tachycardia in patients with atrial fibrillation receiving digitalis

The safety and efficacy of oral verapamil to control exercise tachycardia in 27 patients with atrial fibrillation and 3 with atrial flutter receiving digitalis was evaluated in a double-blind, randomized, crossover study. The heart rate in patients who received verapamil compared with placebo group was lower at rest (mean 69 +/- 13 versus 87 +/- 20 beats/min, p less than 0.01), as was the degree of tachycardia at the end of 3 minutes of a standardized exercise test (104 +/- 14 versus 136 +/- 23 beats/min, p less than 0.01). Doses of verapamil required to achieve suppression of tachycardia were 240 mg/day in 18 patients, 320 mg/day in 6 patients, and 480 mg/day in 3 patients. Only 3 patients complained of adverse effects from verapamil during the double-blind phase of the study. Two patients were discontinued from the study because of adverse reactions. No clinically significant changes during verapamil therapy were observed on the electrocardiogram, chest roentgenogram, echocardiogram or in the laboratory evaluation. Digoxin blood levels were higher in patients who received concomitant verapamil compared with placebo (1.23 +/- 0.59 versus 0.85 +/- 0.46 ng/ml, p less than 0.01), but no patient had signs or symptoms of digitalis toxicity. Thus, oral verapamil given in addition to digitalis is a safe and effective agent in the treatment of patients with chronic atrial fibrillation or flutter to decrease exercise-induced tachycardia.