Volume-dependent factors in hypertension in chronic renal failure.
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Extracellular Space↗
Biomedical subjects
G Fasoli
Publications and source records attributed to G Fasoli.
Myocardial dysfunction and abnormal left ventricular exercise response in autonomic diabetic patients.
In diabetic patients, the pathophysiologic mechanisms of exercise-induced left ventricular (LV) dysfunction remain controversial. In this study, the role of myocardial contractility recruitment in determining an abnormal LV response to isometric or dynamic exercise has been investigated in 14 diabetic patients with autonomic dysfunction. Ischemic heart disease was excluded by the absence of LV wall motion abnormalities induced by isotonic and isometric exercise and by coronary angiography. Left ventricular and myocardial function were studied at rest, and during isometric and isotonic exercise, by two-dimensional echocardiography; moreover, recruitment of an inotropic reserve was assessed by postextrasystolic potentiation at rest and at peak handgrip. An abnormal response of LV ejection fraction to isometric (9/14) or to dynamic (8/14) exercise was frequent in study patients. In these patients, baseline myocardial contractility was normal, and the significant increase in ejection fraction by postextrasystolic potentiation indicated a normal contractile reserve (65 +/- 7% vs. 74 +/- 6%, p = 0.001). Nevertheless, the downward displacement of LV ejection fraction-systolic wall stress relationships during exercise suggests an inadequate increase in myocardial contractility. However, the abnormal ejection fraction at peak handgrip was completely reversed by postextrasystolic potentiation (67 +/- 6% vs. 58.1 +/- 10%, p = 0.008), a potent inotropic stimulation independent of the integrity of adrenergic cardiac receptors. A defective inotropic recruitment, despite the presence of a normal LV contractile reserve, plays an important role in deexercise LV dysfunction in diabetic patients with autonomic neuropathy.
Adult↗
Correlation between cardiac involvement and CTG trinucleotide repeat length in myotonic dystrophy.
OBJECTIVES: Because sudden death due to complete atrioventricular (AV) block or ventricular arrhythmias is the most dramatic event in myotonic dystrophy, we assessed the relation of cardiac disease to cytosine-thymine-guanine (CTG) triplet mutation in adults affected with myotonic dystrophy. BACKGROUND: The myotonic dystrophy mutation, identified as an unstable deoxyribonucleic acid (DNA) sequence (CTG) prone to increase the number of trinucleotide repeats, produces clinical manifestations of the disease in skeletal muscle, the heart and many organ systems. METHODS: Forty-two adult patients underwent electrocardiography and echocardiography; in addition, signal-averaging electrocardiography was performed in 22, and 24-h Holter monitoring was recorded in 32. The diagnosis was established by neurologic examination, electromyography, muscle biopsy and DNA analysis. The patients were then classified into three subgroups on the basis of the number of CTG trinucleotide repeat expansions: E1 = 18 patients with 0 to 500 CTG repeats; E2 = 12 patients with up to 1,000 repeats; E3 + E4 = 10 patients with up to 1,500 repeats and 2 patients with > 1,500 repeats. RESULTS: The incidence of normal electrocardiographic (ECG) results was found to be significantly different in the three subgroups (55%, 50%, 17% in E1, E2, E3, + E4, respectively, p = 0.04), with the highest values in the group with fewer repeat expansions. The incidence of complete left bundle branch block was also significantly different among the groups (5% in E1, 0% in E2, 42% in E3 + E4 p = 0.01) and was directly correlated with the size of the expansion. A time-domain analysis of the signal-averaged ECG obtained in 12 patients in E1, 4 in E2, 5 in E3 and 1 in E4 showed that abnormal ventricular late potentials were directly correlated with CTG expansion (33% in E1, 75% in E2, 83% in E3 + E4, p = 0.05). Moreover, the incidence of ventricular couplets or triplets showed a positive correlation with size of CTG expansion (0 in E1, 0 in E2, 29% in E3 + E4, chi square 0.02). CONCLUSIONS: Our findings suggest that the involvement of specialized cardiac tissue, accounting for severe AV and intraventricular conduction defects, is related to CTG repeat length. In addition, the presence of abnormal late potentials directly correlates to CTG expansion. Abnormal late potentials, caused by slowed and fragmented conduction through damaged areas of myocardium, represent a substrate for malignant reentrant ventricular arrhythmias. In the future, therefore, molecular analysis of DNA should identify patients with cardiac disease at high risk for development of AV block or lethal ventricular arrhythmias.
Adolescent↗
[From overload to contractile deficiency in valvular cardiopathy].
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Aortic Valve Insufficiency↗
Nifedipine in asymptomatic patients with severe aortic regurgitation and normal left ventricular function.
BACKGROUND: Vasodilator therapy with nifedipine reduces left ventricular volume and mass and increases the ejection fraction in asymptomatic patients with severe aortic regurgitation. METHODS: To assess whether vasodilator therapy reduces or delays the need for valve replacement, we randomly assigned 143 asymptomatic patients with isolated, severe aortic regurgitation and normal left ventricular systolic function to receive either nifedipine (20 mg twice daily, 69 patients) or digoxin (0.25 mg daily, 74 patients). RESULTS: By actuarial analysis, we determined that after six years a mean (+/- SD) of 34 +/- 6 percent of the patients in the digoxin group had undergone valve replacement, as compared with only 15 +/- 3 percent of those in the nifedipine group (P < 0.001). In the digoxin group, valve replacement (in a total of 20 patients) was performed because of left ventricular dysfunction (ejection fraction < 50 percent) in 75 percent, left ventricular dysfunction plus symptoms in 10 percent, and symptoms alone in 15 percent. In the nifedipine group, all six patients who underwent valve replacement did so because of the development of left ventricular dysfunction. In addition, all the patients in both groups who underwent aortic-valve replacement had an increase of 15 percent or more in the left ventricular end-diastolic volume index. After aortic-valve replacement, 12 of the 16 patients (75 percent) in the digoxin group and all six patients in the nifedipine group who had had an abnormal left ventricular ejection fraction before surgery had a normal ejection fraction. CONCLUSIONS: Long-term vasodilator therapy with nifedipine reduces or delays the need for aortic-valve replacement in asymptomatic patients with severe aortic regurgitation and normal left ventricular systolic function.
Adult↗
QT-interval variability in hypertrophic cardiomyopathy patients with cardiac arrest.
We studied long-term variability of QT-dispersion in three patients with hypertrophic cardiomyopathy (Maron III) and ventricular fibrillation. Late potentials were absent on signal-averaged electrocardiogram. ST-segment depression was recorded in all three patients at Holter monitoring, and in two during exercise stress testing, nonsustained ventricular tachycardia was present in only one patient. The maximal correct QT-interval and corrected QT-dispersion (QTcd) were measured retrospectively, both off-drug and under treatment with amiodarone and beta-blocker (two patients), or sotalol alone (one patient). Ten age- and sex-matched normal subjects, and 13 hypertrophic cardiomyopathy patients without ventricular arrhythmias formed the control groups. QTcd-values in the control groups never exceeded 80 ms and mean values of 30.1 +/- 10.1 ms and 44.1 +/- 7.9 ms respectively, were found. During long-term follow-up, QTcd increased progressively in two of the three patients with ventricular fibrillation, and at the time of the event all showed a value > 100 ms. Sotalol, but not the amiodarone reduced QTcd. QTcd seems to be a powerful predictor of ventricular electrical instability in the absence of other specific markers, and a promising guide for effective pharmacological therapy.
Adult↗
Left ventricular function and prognosis after myocardial infarction: rationale for therapeutic strategies.
Prognosis after acute myocardial infarction is strongly associated with left ventricular dysfunction. However, asynergy does not necessarily imply loss of viability and myocardial necrosis. In fact, two different patterns of contractile dysfunction, possibly coexisting, have been shown after acute myocardial infarction: Stunning and hibernation represent distinct patterns of contractile dysfunction that share the character of reversibility. It is noteworthy, then, to identify the presence of these two conditions at the bedside and to develop medical treatment to effect recovery of myocardial dysfunction. This strategy has the potential to ameliorate the outcome of patients after acute myocardial infarction by improving left ventricular function. Beta-blocker therapy significantly reduces mortality and the incidence of reinfarction after an acute myocardial infarction: These benefits result from the prevention of sudden death, the reduction of the extent of myocardial injury during the acute phase, and a further antiischemic action. Nevertheless, beta-blocker therapy increases left ventricular dilatation. Recent experimental and clinical data show that ACE inhibitors confer positive therapeutic effects after myocardial infarction by reducing the extent of left ventricular dilation, by reducing mortality, and by improving the clinical outcome. Not all patients, however, can be subjected to this therapeutical approach because of the possible detrimental effects produced by hypotension and by block of neurohormonal activation, sometimes truly compensatory in the early phase. Therefore, it would be interesting to suggest a combination therapy of a beta-blocker with a vasodilator agent (ACE inhibitor or calcium-channel blocker.
Clinical Trials as Topic↗
The gene for arrhythmogenic right ventricular cardiomyopathy maps to chromosome 14q23-q24.
Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) is a dominantly inherited disorder progressively affecting the myocardium and it is one of the major causes of juvenile sudden death. The chromosomal localization of the disease gene is reported here for the first time. A maximum lod score of 6.04 was obtained at theta = 0 for linkage with the polymorphic marker D14S42 (14q23-q24) in two families, one of which has 82 subjects (19 affected) in four generations. The pre-symptomatic identification of ARVD carriers by linkage analysis in the affected families strongly increases the possibility of prevention of life-threatening complications.
Arrhythmias, Cardiac↗
[Appendicular mucocele. A report of a case diagnosed preoperatively].
Mucocele of the appendix is an unusual clinical entity. Despite a recognized constellation of findings, the diagnosis is not usually made prior to surgical exploration. A 35 year old man is reported in whom clinical evaluation, including US and CT scans, resulted in the correct preoperative diagnosis confirmed at surgery and leading to appropriate operative decisions.
Adult↗
Reversible contractile dysfunction of viable myocardium. Implications for decision making process in post-infarction patients.
Myocardial dysfunction and silent myocardial ischemia have been identified as important prognostic factors following acute myocardial infarction, also in low risk patients. In postinfarction patients, impaired left ventricular function is the result of fixed scar and reversible contractile dysfunction of viable stunning or hibernating myocardium. Post-extrasystolic potentiation (PESP) during 2-dimensional echocardiographic monitoring may be used to detect the presence of viable myocardium in asynergic myocardial segments. Incidence of reversible contractile dysfunction is a very common phenomenon at predischarge examination after myocardial infarction in asymptomatic patients, and it is independent on the persistence of silent ischemia. A progressive loss of myocardial viability occurs over the first year following the acute phase despite the maintenance of an asymptomatic clinical status. This phenomenon is associated with significant dilatation of the left ventricle. Moreover, silent ischemia is strongly related with this progressive loss of myocardial viability and left ventricular dilatation. Thus, it becomes evident that the most important role of medical and interventional approaches consists of limiting the acute necrosis by reperfusion and in preventing the loss of viable chronically hypoperfused myocardium that appears to be a major factor of left ventricular remodeling and changes over time of prognostication in individual patients. Finally, the presence of viable myocardium by PESP in the arterial zone at risk is highly predictive of 4-year mortality, particularly in patients with low ejection fraction (< 40%), and identifies patients who are suitable candidates for revascularization after myocardial infarction.
Echocardiography↗
Long-term echocardiographic Doppler monitoring of Hancock bioprostheses in the aortic valve position.
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Actuarial Analysis↗
Silent ischemia and loss of reversible myocardial dysfunction following myocardial infarction.
Sixty-seven asymptomatic patients were enrolled after a first uncomplicated myocardial infarction (MI) so as to study the relevance of reversible myocardial dysfunction in determining left ventricular function soon after the acute episodes and 12 months later. Moreover, the potential role of silent ischemia in conditioning the evolutive aspects of contractile dysfunction has been investigated. Postextrasystolic potentiation during two-dimensional echocardiographic (2-D echo) monitoring has been used to detect the presence of viable myocardium in asynergic myocardial segments. Results of electrocardiographic (ECG) ambulatory monitoring at predischarge determined patient groups: Group A included 49 patients without ST changes during monitoring, while Group B included 18 patients with silent ischemia. Incidence of reversible myocardial dysfunction was similar in the two study groups (82 vs. 86%, p = NS). Group B patients were older (59.6 +/- 6.7 vs. 50.6 +/- 10.6 years, p < 0.015) and had lower ejection fractions (EFs, 43.4 +/- 6.4% vs. 51.2 +/- 8.3%, p = 0.026) and higher at-rest wall-motion scores (WMSs, 11.4 +/- 5.9 vs. 7.2 +/- 3.8, p = 0.019). Left ventricular end-diastolic volume (LVEDV) and potentiated WMS did not differ. At 1-year examination, Group B patients exhibited a greater LVEDV index (96 +/- 6.5 vs. 70.7 +/- 14 ml/m2, p < 0.002) with a worsening both in rest and in potentiated wall-motion score index (12.8 +/- 4.6 vs. 5.3 +/- 1.8, p < 0.001; 9.2 +/- 3.6 vs. 4.8 +/- 2.2, p < 0.001, respectively). Left ventricular EF remained significantly depressed in Group B patients (42 +/- 8.7% vs. 55.5 +/- 8.1%, p < 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Anomalous origin of the left coronary artery from the anterior aortic sinus: role of echocardiography.
Sudden death in the young is a dramatic event which can be avoided with a preventive identification of the underlying cause. We report one case in which we identify the anomalous origin of the left coronary artery from the right sinus of Valsalva by transthoracic and transesophageal echocardiography.
Adolescent↗
Long-term echocardiographic evaluation of closed and open mitral valvulotomy.
From 1968 to 1989, 280 patients with post-rheumatic pure mitral stenosis underwent surgical commissurotomy; 134 a closed and 146 an open technique. Follow-up exceeded 15 years in 56.7% of the patients. Echocardiographic analysis was performed in 120 patients and disclosed a larger mitral valve area in patients who underwent open valvulotomy (1.9 +/- 0.5 cm2 vs. 1.5 +/- 0.4 cm2 for the closed technique, P < 0.0002). On the other hand, considering the occurrence of post-surgical mitral regurgitation at a level greater than, or equal to moderate, open valvulotomy produced less favorable results (18.5% vs. 5% for the closed technique, P < 0.01).
Echocardiography↗
Cardiac involvement in Becker muscular dystrophy.
OBJECTIVES: The purpose of this study was to assess the incidence of myocardial involvement and the relation of cardiac disease to the molecular defect at the deoxyribonucleic acid (DNA) or protein level in Becker muscular dystrophy. BACKGROUND: Dystrophin gene mutations produce clinical manifestations of disease in the heart and skeletal muscle of patients with Becker muscular dystrophy. METHODS: Thirty-one patients underwent electrocardiographic and echocardiographic examination and 24-h Holter monitoring. The diagnosis was established by neurologic examination, dystrophin immunohistochemical assays or Western blot on muscle biopsy, or both, and DNA analysis. RESULTS: Electrocardiographic and echocardiographic findings were abnormal in 68% and 62% of the patients, respectively. Right ventricular involvement was detected in 52%. Left ventricular impairment was observed either as an isolated phenomenon (10%) or in association with right ventricular dysfunction (29%). Right ventricular disease was manifested in the teenagers, and an impairment of the left ventricle was observed in older patients. Right ventricular end-diastolic volumes were significantly increased compared with those in a control group. The left ventricular ejection fraction was significantly lower in older patients than in control subjects or younger patients. Life-threatening ventricular arrhythmias were detected in four patients. No correlations were found between skeletal muscle disease, cardiac involvement and dystrophin abnormalities. In our patients, exon 49 deletion was invariably associated with cardiac involvement. Exon 48 deletion was associated with cardiac disease in all but two patients. CONCLUSIONS: The cardiac manifestation of Becker muscular dystrophy is characterized by early right ventricular involvement associated or not with left ventricular impairment. Exon 49 deletion is associated with cardiac disease.
Adolescent↗
Hypertrophic cardiomyopathy with mitochondrial myopathy. A new phenotype of complex II defect.
Two brothers, 25 and 19 years old, were affected by asymmetrical hypertrophic cardiomyopathy. The older brother had waddling gait and weakness of the proximal girdle muscles, while the younger had a broad-based gait and weakness of selected limb girdle muscles. EMG exam was myopathic. Serum enzyme, CPK and aldolase were elevated. Histochemical reactions in muscle revealed "core-like" areas, subsarcolemmal rims of mitochondria and lipid accumulation. Succinate-dehydrogenase stain showed a lack of activity in both biopsies, with the exception of intrafusal fibers. Microphotometric quantitative measurements confirmed the defect in both biopsies. Biochemical measurements of several mitochondrial enzymes in muscle showed a reduced activity of succinate-dehydrogenase (33%) and succinate-cytochrome C reductase (36-47%) which are both components of complex II. On myocardial biopsy lipid and mitochondrial abnormalities were found. This mitochondriopathy represents a new phenotype of partial complex II defect.
Adult↗
Cardiac fibroma and heart transplantation.
Successful orthotopic heart transplantation was performed in a 38-day-old child with a fetal echocardiographic diagnosis of a left ventricular mass and in a 40-year-old woman with cardiac murmur since childhood and an echocardiographic diagnosis of asymmetric septal hypertrophy. Pathologic examination of the removed hearts, consisting of gross, histologic, immunohistochemical, and ultrastructural studies, led to the final diagnosis of cardiac fibroma. Both patients were alive and in good condition at 35 and 28 months, respectively, after operation.
Adult↗
Tricuspid valve endocarditis: repair with the use of artificial chordae.
We report on a patient who developed tricuspid valve endocarditis on a permanent endocardial pacemaker lead. At operation the endocardial lead was removed and accurate debridement of the tricuspid tissue was performed. Tricuspid valve reconstruction included commissural plication and the construction of artificial polytetrafluoroethylene chordae from the anterior leaflet to the anterior papillary muscle to obtain valve competence.
Aged↗