[Sudden death during Holter monitoring: heart rupture in a patient with a pacemaker].
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Biomedical subjects
Publications and source records attributed to F Loperfido.
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Transmitral pressure half time (PHT) was assessed by continuous wave Doppler in 44 patients with rheumatic mitral valve stenosis (14, pure mitral valve stenosis; 15, combined mitral stenosis and regurgitation; and 15 with associated aortic valve regurgitation). The mitral valve area, derived from transmitral pressure half time by the formula 220/pressure half time, was compared with that estimated by cross sectional echocardiography. The transmitral pressure half time correlated well with the mitral valve area estimated by cross sectional echocardiography. The correlation between pressure half time and the cross sectional echocardiographic mitral valve area was also good for patients with pure mitral stenosis and for those with associated mitral or aortic regurgitation. The regression coefficients in the three groups of patients were significantly different. Nevertheless, a transmitral pressure half time of 175 ms correctly identified 20 of 21 patients with cross sectional echocardiographic mitral valve areas less than 1.5 cm2. There were no false positives. The Doppler formula significantly underestimated the mitral valve area determined by cross sectional echocardiography by 28(9)% in 19 patients with an echocardiographic area greater than 2 cm2 and by 14.8 (8)% in 25 patients with area of less than 2 cm2. In thirteen patients with pure mitral valve stenosis Gorlin's formula was used to calculate the mitral valve area. This was overestimated by cross sectional echocardiography by 0.16 (0.19) cm2 and underestimated by Doppler by 0.13 (0.12) cm2. Continuous wave Doppler underestimated the echocardiographic mitral valve area in patients with mild mitral stenosis. The Doppler formula mitral valve area = 220/pressure half time was more accurate in predicting functional (haemodynamic) than anatomical (echocardiographic) mitral valve area.
Some recent studies suggest that changes in the endogenous opioid peptides (POE) secretion during stress may be involved in various hemodynamic, respiratory and hormonal responses to exercise. To evaluate the relationship between fitness and POE release, 10 mixed-type exercise trained athletes (A) and 10 sedentary normal controls (C) were examined by bicycle stress testing; maximum oxygen uptake (VO2max) and peak work load (PWL) were greater in A than C (VO2max = 61.8 +/- 5.2 vs 40.2 +/- 6.1 ml/kg; PWL = 1525 +/- 229 vs 915 +/- 305 kgm.both p less than 0.01). After 24 hours A and C underwent rectangular bicycle stress testing (two 20' steps at 60% and 80% VO2max). Total plasmatic beta-endorphin (BEP) and its precursor beta-lipotropin (BLPH) were dosed by radioimmunoassay at rest, at 60% VO2max, at 80% VO2max and after complete recovery. Physical exercise caused a transient rise of BEP + BLPH plasma levels in both A and C. In A the increase was greater and occurred earlier than in C. The POE release under submaximal exercise showed a close correlation with oxygen uptake and therefore with fitness. This relation appeared in A at both low and high effort levels, whereas in C it was more strict at higher effort level. There results suggest that POE system play an important role in the adaptive mechanisms in sport practice.
In 72 patients with previous myocardial infarction (MI), mitral regurgitation (MR) was assessed by pulsed-wave Doppler echocardiography and compared with physical and 2-dimensional echocardiographic findings. MR was found by Doppler in 29 of 42 patients (62%) with anterior MI, 11 of 30 (37%) with inferior MI (p less than 0.01) and in none of 20 normal control subjects. MR was more frequent in patients who underwent Doppler study 3 months after MI than in those who underwent Doppler at discharge (anterior MI = 83% vs 50%, p less than 0.01; inferior MI = 47% vs 27%, p = not significant). Of 15 patients who underwent Doppler studies both times, 3 (all with anterior MI) had MR only on the second study. Of the patients with Doppler MR, 12 of 27 (44%) with a left ventricular (LV) ejection fraction (EF) greater than 30% and 1 of 13 (8%) with an EF of 30% or less (p less than 0.01) had an MR systolic murmur. Mitral prolapse or eversion and papillary muscle fibrosis were infrequent in MI patients, whether or not Doppler MR was present. The degree of Doppler MR correlated with EF (r = -0.61), LV systolic volume (r = 0.47), and systolic and diastolic mitral anulus circumference (r = 0.52 and 0.51, respectively). Doppler MR was present in 24 of 28 patients (86%) with an EF of 40% or less and in 16 of 44 (36%) with EF more than 40% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Electrocardiographic (ECG) and vectorcardiographic (VCG) QRS voltage criteria have been analyzed in 26 patients with inferior and 17 with posterior myocardial infarction (MI) in comparison with left ventricular (LV) mass and global and regional wall motion as assessed by M-mode and two-dimensional (2D) echocardiography. Transverse plane QRS maximal vector correlated significantly with LV mass in patients with both inferior and posterior MI (r = 0.65 and 0.87, respectively, p less than 0.01). A transverse plane QRS maximal vector greater than 1.5 mV correctly recognized 12 of 15 (80%) and 9 of 12 (75%) patients with respectively inferior and posterior MI and LV mass greater than 221 gm. Of the ECG measurements, S V1-2 + R V5-6 correlated moderately with LV mass in patients with inferior MI (r = 0.47), and R V1-2 + R V5-6 correlated moderately with LV mass in those with posterior MI (r = 0.67). ECG and VCG QRS voltage data did not correlate with global and regional LV function as assessed by M-mode and 2D echocardiography. We conclude that: ECG and VCG QRS voltage parameters can be utilized for assessing non-invasively LV enlargement in patients with postero-inferior MI; ECG and VCG QRS voltage parameters should be utilized with caution for analyzing LV function or MI size in postero-inferior MI.
The prevalence, characteristics and clinical significance of ventricular electrical instability with programmed ventricular stimulation was studied in 50 hemodynamically stable patients 17 to 40 days after acute myocardial infarction (AMI) using double extrastimuli at 2- and 10-mA intensity and from 2 right ventricular sites. Ventricular electrical instability was defined as induction of 10 or more consecutive intraventricular reentrant beats. Of 50 patients, 23 (46%) had ventricular electrical instability (10 of these had sustained ventricular tachycardia [VT] induced). No significant differences were observed between patients with and without ventricular electrical instability with respect to age, site of AMI, coronary prognostic index, maximal level of CK, number of narrowed coronary arteries and presence of severe wall motion abnormalities. During a mean follow-up of 11.2 months no patient died suddenly. During repeated Holter recordings patients with ventricular electrical instability had a higher incidence of nonsustained VT than did patients without ventricular electrical instability.
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A 45 year old white man developed transient abnormal Q waves and ST segment elevation preceding left anterior fascicular block during exercise stress testing. The simultaneous disappearance of Q waves and fascicular block suggested that the abnormal Q waves were determined by an early septal conduction defect.
Congestive heart failure developed in a patient with low electrocardiographic QRS voltages, diffuse thickening of the septum and free cardiac wall, and a reduction in left ventricular internal diameter, which suggested an infiltrative heart muscle disease. Histological examination at necropsy showed hypertrophic cardiomyopathy with symmetrical left ventricular hypertrophy. Myocardial disarray of type 1A disorganisation was extensive and equally distributed in the ventricular septum and the left anterior and left posterior ventricular free walls. Severe fibrosis (40%) was also present and may have been a possible cause of the electrocardiographic abnormalities as well as of the lack of ventricular dilatation.
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Pulsed Doppler echocardiography was tested to assess the degree of tricuspid regurgitation (TR), classified by right ventriculography, in 47 patients. Forty-eight subjects without TR served as controls (39 with sinus rhythm and 9 with atrial fibrillation). Two Doppler methods were used: the distance of systolic turbulence within right atrium from the tricuspid plane and the quantitative analysis of the flow-velocity traces from the hepatic veins (HVs). Right atrial systolic turbulence was found in 41 of 47 patients with TR and in none of the control subjects, and moderately correlated with the angiographic grading (r = 0.57). In control subjects, TR flow-velocity traces from the HVs showed 2 anterograde flow waves, systolic and diastolic. The ratio of anterograde systolic/anterograde diastolic velocity was more than 0.6 in 38 subjects with sinus rhythm and in 8 with atrial fibrillation. Twenty-two control subjects had a positive wave (designated as "v") coincident with the end of T wave. In 30 patients with TR, a retrograde holosystolic wave was present. Of the remaining patients, 12 had a ratio of anterograde systolic/anterograde diastolic velocity less than 0.6. Fifteen had an end-systolic "v-like" wave, which occurred earlier than the v wave in control subjects (p less than 0.001). In patients with TR, maximal velocities of the anterograde diastolic and retrograde systolic flow correlated with angiographic grading (r = 0.74 and 0.73, respectively). An anterograde diastolic flow velocity more than 26 cm/s and a retrograde systolic flow velocity more than 16 cm/s excluded mild TR. Analysis of Doppler recordings of the HVs is valuable to semiquantitatively assess TR, complementing the right atrial Doppler findings.
Multiform ventricular ectopic rhythm (MVER), i.e., at least two QRS configurations of ventricular ectopic beats (VEBs), was assessed by 24-hour ambulatory ECG recording in four patients with ventricular parasystole (VP). In two of these four patients, VEBs with fixed coupling to the preceding impulses coexisted with VP beats of different configuration. In case no. 1, the VEBs had an identical coupling interval to sinus beats and VP beats, suggesting a mechanism of reentry elicited from both dominant pacemakers. In case no. 2, an intermittent form of VP due to type II second-degree entrance block was present. In this patient, the VEBs were coupled to sinus beats and to sinus-VP fusion beats and appeared to be dependent on the sinus beats reaching the VP focus. A mechanism of reentry determined by the penetration of sinus beats into the VP area, with prematurity-dependent aberrancy of VEBs, was suggested for the coupled VEBs in this patient. These observations suggest that the coexistence of an automatic ventricular ectopic focus and of a reentrant activity determined by, or elicited from, an area of automaticity may constitute the underlying mechanism of MVER in some patients.
The case of a 31-year-old woman with severe right heart failure in the course of bacterial endocarditis and systolic and diastolic murmur at the third left intercostal space is described. Two-dimensional echocardiography showed a vegetation moving from the noncoronary aortic sinus of Valsalva to the right atrium, encroaching upon the septal leaflet of the tricuspid valve. An acquired fistula was confirmed by aortography and surgery. This is an unusual case of tricuspid regurgitation due to acquired aortic sinus of Valsalva-right heart fistula diagnosed by two-dimensional echocardiography.
We describe two patients with probable amyloid infiltrative cardiomyopathy and episodes of syncope. A sick sinus syndrome was suspected by Holter monitoring in both patients. The diagnosis was supported by the finding of a marked prolongation of sinus node recovery time in one case. In both patients a permanent pacemaker was implanted which prevented recurrence of syncopal episodes.
We recently observed a family with tall R waves from V1 to V3 in different relatives, regardless of the actual presence and localization of idiopathic left ventricular hypertrophy.
Thirteen asymptomatic adults less than 40 years old who showed tall right precordial R waves on the ECG were examined by VCG, M-mode and two-dimensional echocardiography (2D Echo). Common causes of QRS anterior displacement, such as right ventricular enlargement or right bundle branch block, were excluded in each subject. Although each subject was normal at physical examination, 2D Echo revealed areas of left ventricular hypertrophy in eight of these 13 subjects. Four had a prevailing hypertrophy of the basal portion of the interventricular septum, three had an isolated apical hypertrophy, and one had a diffuse concentric left ventricular hypertrophy. Results were normal in five cases. 2D Echo classification was confirmed by heart catheterization findings, when available. The subjects with asymmetric septal hypertrophy showed low-voltage QRS leftward forces on the ECG and VCG. ECGs and VCGs were not useful in differentiating the subjects with atypically distributed left ventricular hypertrophy from the normals: high-voltage QRS leftward forces and T wave abnormalities were evident in some subjects of both groups. Tall right precordial R waves may constitute a marker of hypertrophic cardiomyopathy in asymptomatic young adults. 2D Echo is useful to exactly classify these subjects.