Assessment of tricuspid regurgitation by pulsed Doppler ultrasonography of the hepatic veins.

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.

Circadian variation of ventricular tachycardia in acute myocardial infarction.

Circadian rhythms have been described both for acute myocardial infarction (AMI) and sudden death. In this study the diurnal distribution of ventricular tachycardia (VT) in patients with AMI was analyzed. Ninety-four AMI patients with greater than or equal to 1 VT on Holter electrocardiographic monitoring who were not taking antiarrhythmic drugs were studied. Forty-seven patients had a recent AMI (group A) and 47 an old AMI (group B). Chronobiologic analysis was made by single cosinor method. There were 157 VTs (mean 1.67 VTs/patient, range 1 to 10) in the 94 patients: 70 in group A and 87 in group B. A significant circadian rhythm of VT was found in the total population with acrophase at 2:29 P.M. The hourly distribution of VT showed a tendency to bimodality, which seemed due to a different time of peak VT occurrence in group A (significant rhythm with acrophase at 4:40 P.M.) and group B (significant rhythm with acrophase at 12:39 P.M.). Thus, the hourly VT frequency in patients with AMI has a significant circadian variation with the highest occurrence in the awake hours, similar to the rhythms described for AMI and sudden death.

Reproducibility in circadian rhythm of ventricular premature complexes.

To evaluate the existence and reproducibility of a circadian rhythm of ventricular premature complexes (VPCs), 38 patients (mean age 57 +/- 17 years) with greater than or equal to VPCs/hour were studied with 24-hour electrocardiogram Holter monitoring. Nineteen patients had coronary artery disease and 19 had structurally normal hearts. A second Holter electrocardiogram was recorded in all patients from 2 to 47 days (mean 11) after the first. Chronobiologic analysis was made by single and mean cosinor methods. A significant and similar circadian rhythm of VPCs was found in the total sample both on the first (mesor 399, acrophase at 15:08, p less than 0.01) and the second day (mesor 306, acrophase at 14:47, p less than 0.05), with 2 main peaks, the first in the late morning and the second in the afternoon. However, only 18 patients (47%, group A) had a significant individual circadian rhythm of VPCs on both days, whereas 20 (53%, group B) did not have a significant rhythm in greater than or equal to 1 day. A high reproducibility of the circadian rhythm of VPCs was found in group A patients, with a difference of 2.1 +/- 1.8 hours between the acrophases of the 2 days, whereas the difference was 4.4 +/- 3.3 hours in group B patients (p less than 0.01). Among group A patients, 14 (78%) had a VPC rhythm with acrophase occurring during waking hours, whereas the acrophase of 4 (22%) occurred during the night. The reproducibility of the circadian rhythm of VPCs was not influenced by gender, presence of coronary disease, medical therapy, basal VPC number, or day-to-day variability of VPCs, although group A patients were older than group B patients (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular arrhythmia induced by programmed ventricular stimulation after acute myocardial infarction.

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.

Pulsed Doppler echocardiographic analysis of mitral regurgitation after myocardial infarction.

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)

Persisting hypereosinophilia and myocardial activity in the fibrotic stage of endomyocardial disease.

An unusual case of endomyocardial fibrosis is reported complicating an idiopathic hypereosinophilic syndrome. Persisting hypereosinophilia, degranulated eosinophils in the blood, and myocardial activity have been found accompanying the fibrotic phase of endomyocardial disease. This occurrence supports the unitarian theory on tropical and temperate endomyocardial disease and suggests in such a condition the use of steroids or cytotoxic drugs in addition to surgery.

Rhythm of carnitine levels in serum and urine of normal subjects.

A study of the diurnal serum and urine levels of L-carnitine and acetylcarnitine was carried out in eleven healthy volunteers. No significant difference was found between the levels in the morning and in the afternoon, although a higher carnitinaemia was shown in the waking hours when the energy demands were higher.

Extension of calcific deposits in the anterior mitral valve leaflet and mitral valve stenosis severity. Use of 2D Echo parasternal long-axis view.

To evaluate the role of the extent of calcific deposits on the anterior mitral leaflet in predicting the severity of mitral valve stenosis, two-dimensional echocardiography (2D Echo) and heart catheterization data were analysed in 62 patients with mitral valve stenosis, pure or associated with trivial valve regurgitation. 50 patients had technically adequate 2D Echo. Of these, 28 had pure mitral valve stenosis. The mitral valve area was estimated from the parasternal short-axis 2D Echo projection. Using the parasternal long-axis projection, calcium deposits location and extension on the anterior mitral leaflet was examined. Patients were subdivided into the following groups: Group 0 (absence of calcium deposits = 19 patients), Group 1 (calcium on distal third of the leaflet = 19 patients), Group 2 (calcium on mid and distal segments = 11 patients), Group 3 (calcium on the entire leaflet = one patient). The extension of calcium deposits in long-axis projection was contrasted with 2D Echo mitral valve area in the 50 mitral valve patients. 2D Echo and heart catheterization derived mitral valve area were compared to each other in the 28 patients with pure mitral valve stenosis. 2D Echo mitral valve area was greater in Group 0 patients (1.8 +/- 0.4 cm2) than in Group 1 (1.4 +/- 0.4 cm2) and in Group 2 (1.1 +/- 0.3 cm2) (p less than 0.001 between the three groups). Calcific deposits were present on the anterior mitral leaflet in 30/31 patients with 2D Echo mitral valve area less than or equal to 2 cm2. However, of the 19 patients of Group 0, 13 had moderate and one severe mitral valve stenosis. In the 28 patients with pure mitral valve stenosis, 2D Echo mitral valve area was excellently correlated with Gorlin's derived mitral valve area (r = 0.90). However, in patients with extensive calcification of the anterior mitral valve leaflet (Group 2), 2D Echo mitral valve area was significantly greater than the Gorlin's derived area (1.08 +/- 0.20 cm2 versus 0.68 +/- 0.17 cm2; p less than 0.001). In four patients of Group 2, the mitral valve stenosis was moderate by 2D Echo grading and severe by heart catheterization data. Our data suggest that the study of extension of calcific deposits on the anterior mitral valve leaflet may be a complementary aid in quantifying mitral valve stenosis to the 2D Echo mitral valve area estimate, especially when the valve is severely calcified.

Coenzyme Q10 in dilated cardiomyopathy.

The authors have tried to study the therapeutic efficacy of coenzyme Q10 (CoQ10) in patients with dilated cardiomyopathy (DCM). In fact, CoQ10 has been shown to be deficient in myocardial tissue biopsies taken from DCM hearts, compared to normal hearts. Thirty patients with histological diagnosis of DCM were orally treated with CoQ10 (100 mg/die) for 2 months. Before and after treatment a clinical examination with determination of NYHA class and an echocardiographic examination with determination of ejection fraction (EF) and of telediastolic (TDV) and telesystolic (TSV) volumes were performed, and blood was drawn for plasma CoQ10 determination. In seven patients the pretreatment endomyocardial level of CoQ10 was also assayed. Seven patients left the study because of poor therapeutic compliance. In 47% of patients the clinical symptomatology regressed, with improvement of NYHA class. The EF improved from 0.31 +/- 0.09 to 0.37 +/- 0.11 (p less than 0.001). The TDV passed from 262.2 +/- 85 ml to 203.3 +/- 83 ml (p less than 0.05), and the TSV from 166.13 +/- 75 ml to 126.9 +/- 56 ml (ns). The CoQ10 plasmatic levels improved in 95% of the patients: from 0.74 +/- 0.37 micrograms/ml to 2.27 +/- 0.99 micrograms/ml (p +/- 0.0001). The CoQ10 myocardial levels did not show univocal values, but the patients with lower myocardial levels seemed to have a better therapeutic response. These data suggest that the CoQ10 deficiency in DCM may be reversible and that the therapeutic effects depend on the basal plasmatic and myocardial levels. Therapy with coenzyme Q10 may be considered to be an efficacious aid in the traditional treatment of chronic cardiac failure.

[Circadian rhythm of the heart rate and autonomic nervous system stimulation tests in patients with systemic lupus erythematosus]. / Ritmo circadiano della frequenza cardiaca e prove di stimolazione autonomica in pazienti con lupus eritematoso sistemico.

We studied 19 women (mean age 35 +/- 13 years) with systemic lupus erythematosus (SLE), in order to evaluate whether or not alterations in the circadian rhythm of heart rate (HR) occur in patients with pathologic responses to stimulation tests of the autonomic nervous system (ST-ANS). The duration of SLE was 5.3 +/- 5 years. None of the patients had clinical signs of cardiopathy or dysautonomy, nor were any of them taking drugs with known effects on the heart or ANS. Nine patients (47%, group A) had normal ST-ANS and 10 (53%, group B) had an abnormal response to at least 1 ST-ANS (5 to sympathetic ANS, 3 to parasympathetic and 2 to both ST-ANS). Age, duration of disease and therapy were not different between the 2 groups. All patients underwent 24-hour ambulatory ECG monitoring, and chronobiologic analysis of hourly HR was carried out by single and mean cosinor methods. A significant circadian rhythm was found both in the total sample (mesor 80 b/min, acrophase h 13:12; p less than 0.01), and, separately, in group A (mesor 82 b/min, acrophase h 13:11; p less than 0.01) and group B (mesor 78 b/min, acrophase h 13:12; p less than 0.01). No difference existed between the HR circadian rhythms of the 2 groups. Thus, our data show the possibility of ANS involvement in SLE patients without clinical signs of dysautonomy; the analysis of the HR circadian rhythm does not appear to be a sensitive method to identify early involvement of the ANS in these patients.