Role of echocardiography in the assessment of left ventricular thrombus embolic potential after anterior acute myocardial infarction.

The contribution of cardiac ultrasound in assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction was verified in a prospective study of serial echocardiograms (mean, 18.9 examinations per patient) obtained over a long-term period (1-72 months; mean, 38±12). The study population comprised 222 patients (162 men; age, 64±11 years) with a first anterior acute myocardial infarction, treated with thrombolysis (group A) or receiving no antithrombolic therapy (group B). Embolism occurred in a total of 12 patients (11 with a left ventricular thrombus; p<0.005) and was more frequent in group B (10 patients; p<0.04). Predictors of embolism were the absence of thrombolysis, detection of a left ventricular thrombus, protrusion or mobility of the thrombus, and morphologic changes in the thrombus over time. Patients in group A had a lower incidence of each of these predictors, and a higher thrombus resolution rate. An appropriate echocardiographic protocol is crucial to assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction and may help to identify candidates for aggressive antithrombotic therapy (c)2001 CHF, Inc.

Epidemiology of hypertrophic cardiomyopathy-related death: revisited in a large non-referral-based patient population.

BACKGROUND: Death resulting from hypertrophic cardiomyopathy (HCM), particularly when sudden, has been reported to be largely confined to young persons. These data emanated from tertiary HCM centers with highly selected referral patterns skewed toward high-risk patients. METHODS AND RESULTS: The present analysis was undertaken in an international population of 744 consecutively enrolled and largely unselected patients more representative of the overall HCM spectrum. HCM-related death occurred in 86 patients (12%) over 8+/-7 years (mean+/-SD). Three distinctive modes of death were as follows: (1) sudden and unexpected (51%; age, 45+/-20 years); (2) progressive heart failure (36%; age, 56+/-19 years); and (3) HCM-related stroke associated with atrial fibrillation (13%; age, 73+/-14 years). Sudden death was most common in young patients, whereas heart failure- and stroke-related deaths occurred more frequently in midlife and beyond. However, neither sudden nor heart failure-related death showed a statistically significant, disproportionate age distribution (P=0.06 and 0.5, respectively). Stroke-related deaths did occur disproportionately in older patients (P=0.002). Of the 45 patients who died suddenly, most (71%) had no or mild symptoms, and 7 (16%) participated in moderate to severe physical activities at the time of death. CONCLUSIONS: HCM-related cardiovascular death occurred suddenly, or as a result of heart failure or stroke, largely during different phases of life in a prospectively assembled, regionally based, and predominantly unselected patient cohort. Although most sudden deaths occurred in adolescents and young adults, such catastrophes were not confined to patients of these ages and extended to later phases of life. This revised clinical profile suggests that generally held epidemiological tenants for HCM have been influenced considerably by skewed reporting from highly selected populations. These data are likely to importantly affect risk stratification and treatment strategies importantly for the prevention of sudden death in HCM.

Magnitude of left ventricular hypertrophy and risk of sudden death in hypertrophic cardiomyopathy.

BACKGROUND: Sudden death is known to be a possible consequence of hypertrophic cardiomyopathy. Quantification of the risk of sudden death, however, remains imprecise for most patients with this disease. METHODS: We assessed the relation between the magnitude of left ventricular hypertrophy and mortality in 480 consecutive patients with hypertrophic cardiomyopathy. The patients were categorized into five subgroups according to maximal wall thickness: 15 mm or less, 16 to 19 mm, 20 to 24 mm, 25 to 29 mm, and 30 mm or more. Their ages ranged from 1 to 89 years (median, 47). RESULTS: Over a mean follow-up period of 6.5 years, 65 of the 480 patients (14 percent) died: 23 suddenly, 15 of heart failure, and 27 of noncardiac causes or stroke. The risk of sudden death increased progressively and in direct relation to wall thickness (P=0.001), ranging from 0 per 1000 person-years (95 percent confidence interval, 0 to 14.4) for a wall thickness of 15 mm or less to 18.2 per 1000 person-years (95 percent confidence interval, 7.3 to 37.6) for a wall thickness of 30 mm or more and almost doubling from each wall-thickness subgroup to the next. The cumulative risk 20 years after the initial evaluation was close to zero for patients with a wall thickness of 19 mm or less but almost 40 percent for wall thicknesses of 30 mm or more. As compared with the other subgroups, patients with extreme hypertrophy were the youngest (mean age, 31 years), and most (41 of 43) had mild symptoms or no symptoms; of the 12 patients who were less than 18 years old at the initial evaluation, 5 died suddenly. CONCLUSIONS: In hypertrophic cardiomyopathy, the magnitude of hypertrophy is directly related to the risk of sudden death and is a strong and independent predictor of prognosis. Young patients with extreme hypertrophy, even those with few or no symptoms, appear to be at substantial long-term risk and deserve consideration for interventions to prevent sudden death. The majority of patients with mild hypertrophy are at low risk and can be reassured regarding their prognosis.

Infective endocarditis in hypertrophic cardiomyopathy: prevalence, incidence, and indications for antibiotic prophylaxis.

BACKGROUND: The literature on infective endocarditis in hypertrophic cardiomyopathy (HCM) is virtually confined to case reports. Consequently, the risk of endocarditis in HCM remains undefined. METHODS AND RESULTS: We assessed the occurrence of endocarditis in 810 HCM patients evaluated between 1970 and 1997. Endocarditis was diagnosed in 10 patients, 2 of whom were excluded from analysis of prevalence and incidence because they were referred for acute endocarditis. At first evaluation, echocardiographic features consistent with prior endocarditis were identified in 3 of 808 patients, a prevalence of 3.7 per 1000 patients (95% CI, 0.8 to 11). Of 681 patients who were followed, 5 developed endocarditis, an incidence of 1.4 per 1000 person-years (95% CI, 0.5 to 3.2); outflow obstruction was present in each of these 5 patients and was associated with the risk of endocarditis (P=0.006). In the 224 obstructive patients, incidence of endocarditis was 3.8 per 1000 person-years (95% CI, 1.6 to 8.9) and probability of endocarditis 4. 3% at 10 years. Left atrial size was also associated with the risk of endocarditis (P=0.007). In patients with both obstruction and atrial dilatation (>/=50 mm), incidence of endocarditis increased to 9.2 per 1000 person-years (95% CI, 2.5 to 23.5). Analysis of all 10 patients with endocarditis identified outflow obstruction in each and atrial dilatation in 7. CONCLUSIONS: Endocarditis in HCM is virtually confined to patients with outflow obstruction and is more common in those with both obstruction and atrial dilatation. These results indicate that antibiotic prophylaxis is required only in patients with obstructive HCM.

Long-term prospective assessment of left ventricular thrombus in anterior wall acute myocardial infarction and implications for a rational approach to embolic risk.

To prospectively assess the predictive value of left ventricular (LV) thrombus anatomy for defining the embolic risk after acute myocardial infarction (AMI), 2 comparable groups of patients with a first anterior AMI (group A, 97 thrombolysed patients; group B, 125 patients untreated with antithrombotic drugs [total 222]) underwent prospective serial echocardiography (follow-up 39 +/- 13 months) at different time periods. LV thrombi were detected in 26 patients in group A (27%) and in 71 in group B (57%; p <0.005). Embolism occurred in 12 patients (5.4%; 1 in group A [1%] vs 11% in group B [9%], p < 0.04). At multivariate analysis, thrombus morphologic changes were the most powerful predictor of embolism (p <0.001), followed by protruding shape (p <0.01) and mobility (p <0.02). In patients untreated with thrombolysis, a higher occurrence of thrombus morphologic changes (48% vs 8%, p <0.002) and protruding shape (69% vs 31%, p <0.002) were observed, whereas thrombus mobility was similar in the 2 groups (18% vs 8%, p = NS). Thrombus resolution occurred more frequently in thrombolysed patients (85% vs 56%, p <0.002). Thus, after anterior AMI, changes in LV thrombus anatomy frequently occur and appear the most powerful predictor of embolization. A minor prevalence of thrombus, a more favorable thrombus anatomy, and a higher resolution rate may contribute to reduce embolic risk after thrombolysis.

Chronic aneurysmatic dilatation: a possible source of lethal embolization in patients with acute myocardial infarction undergoing thrombolysis.

Left ventricular thrombosis is relatively common after acute myocardial infarction, especially in the anterior site, and represents a possible cause of potentially lethal peripheral embolization 1. Therefore, several studies have been performed in order to assess the efficacy of different antithrombotic drugs in resolving the detected thrombi or reducing their embolic potential. Fibrinolytic agents appear effective in this regard: in the majority of cases, they produce complete lysis and resolution of the thrombi. However, this treatment may itself cause embolic complications by producing a rapid fragmentation of thrombus and the subsequent emission of disrupted portions of the intracardiac mass into the systemic vascular bed [2]. This dramatic effect of thrombolysis has suggested the possibility that even the standard treatment of acute myocardial infarction with fibrinolysis implies a danger of embolization in those patients in whom a left ventricular thrombus may be present either from a previous myocardial infarction or from a very early thrombus development. However, this hypothesis has not yet been confirmed by direct observation. We report the case of a patient with a first acute anterior myocardial infarction, in whom the thrombolytic treatment induced lysis and embolization from a left ventricular thrombus present in an aneurysmatic dilatation of the infero-posterior wall due to a previous inferior myocardial infarction.

Prognosis of asymptomatic patients with hypertrophic cardiomyopathy and nonsustained ventricular tachycardia.

BACKGROUND: In the early 1980s, studies performed in highly selected referral patients with hypertrophic cardiomyopathy reported a strong association between the presence of brief episodes of ventricular tachycardia (VT) on ambulatory ECG monitoring and sudden death. These observations led to antiarrhythmic treatment in many patients with hypertrophic cardiomyopathy and brief episodes of VT. In recent years, however, a growing awareness of the potential arrhythmogenic effects of antiarrhythmic medications has raised doubts regarding such a therapeutic approach, particularly in less selected and lower-risk patient populations. METHODS AND RESULTS: In the present study, we examined the prognostic significance of nonsustained VT in a population of 151 patients with hypertrophic cardiomyopathy who were asymptomatic or had only mild symptoms at the time of their initial ambulatory ECG recording. Of the 151 study patients, 42 had episodes of VT and 109 did not. The runs of VT ranged from 3 to 19 beats, with 35 patients (83%) having < 10 beats. The number of runs of VT ranged from 1 to 12 in 24 hours, with 36 patients (86%) having < or = 5 episodes of VT. Thus, in most patients, the episodes of VT were brief and infrequent. Follow-up averaged 4.8 years. Of the 151 study patients, 6 died suddenly, 3 in the group with VT and 3 in the group without VT. Two other patients, both in the group without VT, died of congestive heart failure. The total cardiac mortality rate was 1.4% per year in the patients with VT (95% CI, 0.4% to 3.5%) and 0.9% in those without VT (95% CI, 0.4% to 2.0%; P = .43). The relative risk of cardiac death for patients with VT was 1.4 compared with patients without VT (95% CI, 0.6 to 6.1). The sudden death rate was 1.4% per year in the patients with VT (95% CI, 0.4% to 3.5%) and 0.6% in those without VT (95% CI, 0.2% to 1.5%; P = .24). The relative risk of sudden death for patients with VT compared with those without VT was 2.4 (95% CI, 0.5 to 11.9). Of the 151 patients included in the study, 88 (58%) remained asymptomatic and were not treated with cardioactive medications during follow-up. Of these 88 patients, 20 were in the group with VT and 68 in the group without VT. None of these patients died. CONCLUSIONS: Our results show that cardiac mortality is low in patients with hypertrophic cardiomyopathy who are asymptomatic or only mildly symptomatic and have brief and infrequent episodes of VT on ambulatory ECG monitoring. Our findings also suggest that brief and infrequent episodes of VT should not be considered, per se, an indication for antiarrhythmic treatment in such patients.

Morphology of the "athlete's heart" assessed by echocardiography in 947 elite athletes representing 27 sports.

In the present study, we used echocardiography to investigate the morphologic adaptations of the heart to athletic training in 947 elite athletes representing 27 sports who achieved national or international levels of competition. Cardiac morphology was compared for these sports, using multivariate statistical models. Left ventricular (LV) diastolic cavity dimension above normal (> 54 mm, ranging up to 66 mm) was identified in 362 (38%) of the 947 athletes. LV wall thickness above normal (> 12 mm, ranging up to 16 mm) was identified in only 16 (1.7%) of the athletes. Athletes training in the sports examined showed considerable differences with regard to cardiac dimensions. Endurance cyclists, rowers, and swimmers had the largest LV diastolic cavity dimensions and wall thickness. Athletes training in sports such as track sprinting, field weight events, and diving were at the lower end of the spectrum of cardiac adaptations to athletic training. Athletes training in sports associated with larger LV diastolic cavity dimensions also had higher values for wall thickness. Athletes training in isometric sports, such as weightlifting and wrestling, had high values for wall thickness relative to cavity dimension, but their absolute wall thickness remained within normal limits. Analysis of gender-related differences in cardiac dimensions showed that female athletes had smaller LV diastolic cavity dimension (average 2 mm) and smaller wall thickness (average 0.9 mm) than males of the same age and body size who were training in the same sport.(ABSTRACT TRUNCATED AT 250 WORDS)

Dipyridamole echocardiographic test performed 3 days after an acute myocardial infarction: feasibility, tolerability, safety and in-hospital prognostic value.

In recent years, increasing evidence has pointed to the potential of dipyridamole stress echocardiography as a fast, effective, inexpensive method of risk stratification after an acute myocardial infarction. A very early stratification by this test could improve the patient's management and reduce the duration of in-hospital stay, and, thus, the costs. Two-hundred and fifty-one consecutive patients (208 male, age 58 +/- 11) with a two-dimensional echocardiogram of good technical quality underwent a dipyridamole echocardiographic test (DET) 70 +/- 6 h after an acute myocardial infarction. Criterion for positivity was the identification of a transient regional asynergy that was absent or of a lower degree in the baseline examination. Positivity was defined as 'at low-dose' or 'at high-dose' if the asynergy was detected before or after the 8th min of a drug infusion. All tests were performed without any major side effects. DET was positive in 149 (59%) and negative in 102 (41%) patients. During the hospital stay, cardiac events (death, reinfarction, angina) occurred in 52/251 patients: in 49/149 with a positive and in 3/102 with a negative test (sensitivity 94%, negative predictive value 97%, P < 0.00001). Severe events (death and reinfarction) occurred in 14/251: in 12/149 with a positive DET and in 2/102 with a negative DET (sensitivity 86%; negative predictive value: 98%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Sixty-six episodes of ventricular fibrillation within four hours: electrical stability restored by propafenone.

Ventricular fibrillation is a complication in patients hospitalized for acute myocardial infarction. We report the case of an unusually high number of episodes of ventricular fibrillation (66 episodes) that occurred within a period of 4 h in a patient with recent anterior myocardial infarction. In patients with acute or recent myocardial infarction and recurrent episodes of ventricular fibrillation, intravenous lidocaine is the antiarrhythmic medication of choice. In our patient, recurrences of ventricular fibrillation were not prevented either by lidocaine, or amiodarone. The rate of recurrence of ventricular fibrillation, however, decreased dramatically, twice, in the minutes following two separate boluses of propafenone, and the arrhythmia did not recur when continuous infusion of propafenone was started. We cannot exclude that were the combined antiarrhythmic effects of lidocaine, amiodarone and propafenone that led to the final control of the arrhythmia.

Atrial natriuretic peptide response is blunted in patients with acute myocardial infarction and mild left ventricular dysfunction.

Neurohumoral parameters in 45 asymptomatic patients with acute myocardial infarction were measured. In patients with mild left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mm Hg), atrial natriuretic peptide levels differed significantly from those in patients with normal left ventricular function (127 +/- 74 pg/ml vs. 79 +/- 71 pg/ml; p < 0.001). After stimulus an increase in atrial natriuretic peptide levels (79 +/- 71 to 118 +/- 86 pg/ml; p < 0.001) was found only in patients with normal hemodynamic parameters. These data show that in patients with left ventricular dysfunction, the atrial natriuretic system is activated; however, atrial natriuretic peptide response to stimulus is present only in patients with normal hemodynamics.

Selective activation of atrial natriuretic peptide in patients with myocardial infarction and mild left ventricular dysfunction.

The purpose of this study was to investigate whether neurohumoral activation occurs in asymptomatic patients with acute myocardial infarction (AMI) and without clinical signs of heart failure. During the early phase of AMI (mean 8 days), the neurohumoral profiles of 60 patients (mean age 59 range 37 to 70) were examined. Blood levels of the following humoral parameters were measured: atrial natriuretic peptide (ANP), plasma renin activity, aldosterone and vasopressin. All patients underwent cardiac catheterization during hospitalization. Baseline hemodynamic characteristics identified left ventricular dysfunction (ejection fraction < or = 45% and/or left ventricular end-diastolic pressure > or = 15 mmHg) in 32 patients; the remaining 28 patients had normal hemodynamic parameters. In patients with AMI, plasma ANP levels differed significantly from control subjects (111 +/- 74 pg/ml vs. 53 +/- 18 pg/ml; P < 0.001). In patients with AMI and mild left ventricular dysfunction ANP levels were significantly increased when compared to patients with AMI and normal left ventricular function (129 +/- 73 pg/ml vs. 82 +/- 69 pg/ml; P < 0.001). The hemodynamic data showed a significant correlation with ANP only in patients with AMI and left ventricular dysfunction (EF% r = 0.42; LVEDP r = 0.44; P < 0.001). These data show that in patients with myocardial infarction and without heart failure, the atrial natriuretic peptide is the only neurohumoral system activated out of all neurohumoral systems tested in this population and its circulating levels are strictly related to the degree of left ventricular dysfunction.

Cardiac involvement in thalassaemia major: altered atrial natriuretic peptide levels in asymptomatic patients.

Congestive heart failure is the most common cause of death in young adults with thalassaemia major. In the present study we compared atrial natriuretic peptide levels (ANP) in 30 asymptomatic patients with thalassaemia major (aged 16.6 +/- 6.4 years), normal left ventricular diastolic cavity dimension and systolic function, with 30 aged and sex matched normal control subjects. ANP levels were significantly higher in patients with thalassaemia major compared to controls (93.9 +/- 26.3 pg.ml-1 vs 51.8 +/- 26.5 pg.ml-1; P < 0.001). Plasmatic renin activity, aldosterone, urinary sodium and catecholamine levels at basal conditions did not differ significantly in these two groups (ns). Blood volume stimulation (blood transfusion) in thalassaemic patients was followed by an increase of mean ANP values (93.9 +/- 26.3 to 109.1 +/- 40.5 pg.ml-1; P < 0.03). ANP basal levels above two standard deviations of the mean values obtained in normal control subjects were considered as abnormal and found to be in close correlation with the presence of diastolic dysfunction of the left ventricle identified by Doppler echocardiography. The method has a 57% sensitivity and a 91% specificity for revealing pre-clinical cardiac involvement (P < 0.02). Although a longer observation period is necessary in order to define the clinical and prognostic significance of these data, our results show that an increase in ANP basal values is present in asymptomatic patients with thalassaemia major. This suggests initial myocardial involvement, while ANP response to volume overload is maintained.