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The aim of this study was to assess the incremental value of tissue harmonic imaging vs conventional echocardiography for evaluating left ventricular ejection fraction by manual and automated quantitation as well as visual estimation in patients with distorted left ventricles.In 25 patients unselected for image quality and with distorted left ventricles who underwent a nuclear study, digital cineloops of standard apical views were acquired by both tissue harmonic imaging and conventional echocardiography and sent to six observers for analysis of visual and quantitative left ventricular ejection fraction. Tissue harmonic imaging improved both the correlation and agreement of all echo techniques with nuclear measures, compared with conventional echocardiography echo, reducing standard errors (SE) to below 10%: for the visual estimate SE=7.5%, for manual tracing SE=6.3% and for automated tracing SE=8%. Tissue harmonic imaging decreased inter-observer variability compared with conventional echocardiography echo for both visual assessment (12.4% vs 18.4%, P0.05) and quantitative measures (for manual tracing, 8.2% vs 11.8%, P0.05; for automated tracing, 7.8% vs 16.8%, P0.05).In patients with distorted left ventricles unselected for image quality, tissue harmonic imaging improves accuracy and reproducibility of both visual and quantitative echocardiographic assessment of left ventricular ejection fraction. In particular, it promotes automated quantitation by reducing its high standard error into a clinically reasonable range.

Epidemiological evidence shows that among women, the incidence of all, including less severe, coronary events is still increasing. However, owing both to diminished lethality as well as the reduction in the rate of acute myocardial infarction, mortality has globally decreased. The strong association observed between mortality and major cardiovascular risk factors as well as between their temporal changes and the occurrence of coronary disease makes the undertaking of multifactorial prevention strategies, including the formulation of risk charts for asymptomatic women and men, necessary. The different "penetrance" of risk factors in women, together with their interaction with female hormones, plays an important role in the development of cardiovascular disease. The excess risk of cigarette smoking is 2-4 times higher in women than in men and the correlation with the number of cigarettes smoked daily is distinct. However, the risk starts to decrease immediately after stopping and after 3-5 years is similar to that of non-smokers. In women, the association between hypertension, coronary artery disease and early mortality is stronger than in men: there is no threshold below which the risk disappears. Diet and lifestyle strongly influence the development of hypertension. For this reason, the American Heart Association/American College of Cardiology guidelines recommend adherence to a set of dietary and lifestyle habits including body weight control and physical activity. In particular, diet may modify the "penetrance" of risk factors in women: hence excess intake of saturated fatty acids associated with decreased cereals, fruit and vegetables does not only alter the lipid profile but also increases the risk of coronary disease. An elevated total/HDL cholesterol ratio and the presence of lipoprotein(a) constitute significant risk factors for coronary events. On the other hand, high HDL cholesterol levels (45 mg/dl) are considered to be protective in women. However, data on the efficacy of strategies aimed at reducing blood LDL levels in hypercholesterolemic women are limited and controversial. Pharmacological therapy is recommended in women with primary familial hypercholesterolemia and during menopause when the patient presents with two or more risk factors. Besides, pharmacological therapy is also indicated for women with a history of coronary artery disease in whom benefits exceed those observed in male patients with a similar clinical picture. In diabetic women, the risk of coronary mortality is increased 3 to 7-fold compared to the 2 to 3-fold increase observed in diabetic men. Diabetes definitely increases the effects of the other risk factors and modifies the protective effect by estrogens. However, to date, there is no evidence that keeping glucose levels within normal limits reduces the risk of coronary artery disease nor has a glycemic threshold capable of predicting mortality risk in diabetic women been established. For this reason, guidelines for such patients are aimed at keeping the other risk factors under strict control in order to significantly reduce their effect. Obesity results in a series of metabolic alterations that increase the risk of cardiovascular disease in both sexes. Although most, if not all, data confirm that obesity alone is not of predictive value, central obesity constitutes a risk factor for cardiovascular disease. A body mass index24.9 kg/m2 and a waist circumference80 cm are recommended so as to decrease the likelihood of developing a menopausal insulin-resistance syndrome. It has been demonstrated that in men, a sedentary lifestyle is correlated with a higher cardiovascular and all-cause mortality; some recent observational studies suggest a 25-30% decrease in the mortality risk for women who perform physical exercise. Current guidelines recommend at least 30 min daily of dynamic moderately vigorous activity, including brisk walking. Rather than to the reduction in the serum levels of endogenous estrogens, the increase in the incidence of disease and of mortality following menopause should be attributed to the age-related modifications in risk factors which result in an increased risk of coronary artery disease. In spite of the proved detrimental effect of estrogen deficiency on LDL- and HDL-cholesterol, on arterial smooth muscle cell proliferation and on insulin secretion and in spite of the data of numerous observational studies and of the HERS trial (all, however, with methodological limitations), clinical evidence does not justify widespread estrogen prescription, not even for purposes of secondary prevention. Besides, the dosages and the route of administration are still subject of debate. (ABSTRACT TRUNCATED)

Echocardiographically recognized resting function, myocardial viability (by low-dose dobutamine) and stress-induced ischemia (by high-dose dipyridamole) are potent predictors of subsequent events, but their relative value in patients evaluated very early after acute myocardial infarction remains to be established.To assess the feasibility and usefulness of an integrated approach with resting and pharmacological stress echo for risk stratification in patients evaluated very early after myocardial infarction.Sixty acute myocardial infarction patients without contraindications to stress testing, and who were being given thrombolytic therapy, underwent resting echo (16-segment model of left ventricle, each segment scored from 1 = normo-hyperkinetic to 4 = dyskinetic), high-dose dipyridamole (up to 0.84 mg/kg over 10') and low-dose dobutamine (up to 10 mcg/kg/min) echo on the third-fourth day after drug withdrawal. The response was "ischemic" with a dipyridamole-induced increase in the regional score1 in segments with a resting score3, and "viable" with a dobutamine-induced decrease in the regional score1 in segments with resting score1. All patients underwent coronary angiography on the tenth-twelfth day after the acute event, and all of them were followed up for 15 +/- 10.04 months.Ischemia elicited by dipyridamole appeared in 29 patients (48%) and dobutamine-induced viability was observed in 28 (47%). Ischemic events occurred in 26 patients (43.4%), five of which during the early in-hospital period. There were three deaths (5%), one re-AMI (1.7%), 7 Canadian Class III-IV angina (12%) and 15 (25%) early revascularization procedures undertaken independently of stress echo results. Events occurred in 21 patients (72%) with dipyridamole-induced ischemia and in 5 (16%) without it (p0.001). Likewise, events occurred in 13 patients (46.4%) with dobutamine-induced inotropic recovery and in 13 (40.6%) without it (p = ns). Event-free survival occurred in 64% of dipyridamole-positive patients, as opposed to 90% of dipyridamole-negative patients (p = 0.025). Dipyridamole echocardiographic test sensitivity and specificity for events were 81 and 74%, respectively. Sensitivity and specificity for events of dobutamine viability were 46 and 55%, respectively. In a multivariate logistic analysis, dipyridamole-induced myocardial ischemia was the strongest predictor of subsequent events (p = 0.01). According to Cox analysis, dipyridamole positivity had a relative risk estimate of 4.Pharmacological stress echo is feasible even very early after acute myocardial infarction via a useful approach based on low-dose dobutamine to assess myocardial viability, and high-dose dipyridamole to assess ischemia. For risk stratification purposes, stress-induced myocardial ischemia outperforms resting function and myocardial viability, and it is independent of angiographic data. Revascularization procedures do not seem to be effective when only viability is present.

Several weeks of prophylactic anticoagulation are routinely prescribed before and after electrical cardioversion of atrial fibrillation. Recent studies have supported the use of transesophageal echocardiography to guide early cardioversion: patients in whom no thrombus is observed are treated with heparin followed by one month of warfarin therapy after the procedure. This kind of treatment requires hospital admission during heparin infusion, because of the need for monitoring partial thromboplastin time.To evaluate if a short at-home treatment (three days) with warfarin is sufficient to reach a good level of anticoagulation, in order to permit safe electrical cardioversion in day-hospital for patients who show no thrombi on transesophageal echocardiography.One hundred twenty-four patients with atrial fibrillation, who were candidates for cardioversion, were treated with warfarin: 10 mg the first and second day, 5 mg the third day in group A patients (n = 79); 15 mg the first day, 10 mg the second and third day in group B patients (n = 45). On the fourth day, INR value was measured and if it was2, warfarin therapy was prolonged until patients reached a good level of anticoagulation. Transesophageal echocardiography was performed when the INR wasor = 2, and patients were cardioverted with DC shock if there were no thrombi. The patients were discharged on the same day of the procedure, and warfarin therapy was continued for 4 weeks there-after. If a thrombus was detected, patients repeated transesophageal echocardiography after 6 weeks of warfarin therapy, and were cardioverted if the thrombus disappeared. Otherwise, cardioversion was deferred and they received prolonged warfarin treatment. If there was poor visualization of the left atrial appendage, patients received conventional warfarin therapy for 3 weeks before and 4 weeks after electrical cardioversion.Mean INR value after three days of warfarin treatment was 2.41 in group A patients and 3.02 in group B patients. Twenty-one patients from group A and 3 patients from group B required anticoagulant therapy for a mean of 3.3 and 5.1 days, respectively, before reaching a good level of anticoagulation (INR valueor = 2). Eight patients reverted spontaneously to sinus rhythm before transesophageal echocardiography. Eighteen thrombi (15.5%) were identified on the transesophageal echocardiography, all of which were in the left atrial appendage. In 11 cases, thrombus disappeared after 6 weeks of warfarin therapy. In 7 patients (6%), the atrial appendage was not sufficiently visualized. Electrical cardioversion was performed on 109 patients and was successful in 88 (80.7%). None of them experienced a clinical thromboembolic event.In the majority of patients in atrial fibrillation, a short at-home warfarin treatment is sufficient to reach a good level of anticoagulation in order to permit safe electrical cardioversion in a day-hospital situation. Larger initial doses can achieve even better results. This treatment algorithm minimizes the anticoagulation period, hospital stay, overall duration of atrial fibrillation and the time required for the mechanical function of the left atrium to return.

Thromboembolic complications after electrical cardioversion (CV) of atrial fibrillation (AF) have been attributed to the dislodgment of preexistent left atrial thrombus during the resumption of atrial contraction. Transesophageal echocardiography (TEE) has been used to identify patients without thrombus, who potentially could undergo CV without anticoagulation. However, embolic events after CV in patients without evidence of thrombus on TEE have recently been reported.To evaluate if absence of thrombi or prethrombotic conditions such as spontaneous echo contrast or left atrial appendage disfunction can justify electrical CV without anticoagulant therapy.Seventy-four patients with AF and candidates for CV underwent monoplane TEE. Patients were cardioverted without anticoagulation in case of: 1) absence of thrombus and/or spontaneous echocardiographic contrast and 2) good visualization of left atrial appendage, with a well defined peak blood flow velocity greater than 20 cm/sec. In all other cases, patients underwent anticoagulant therapy which started 3 weeks before CV and continued for 4 weeks afterwards.Forty-six patients, without thrombus or "prethrombotic" conditions, did not receive anticoagulation, while 28 followed traditional therapy with warfarin. Four patients with a thrombus in the left atrial appendage were identified: 1 died of cerebral embolism 3 days after the beginning of anticoagulation, in another one CV was definitely deferred because of the persistence of thrombus after 1 month of warfarin therapy. One patient, with left atrial appendage disfunction, died suddenly after 5 days of anticoagulation. Two patients reverted spontaneously in sinus rhythm. Two patients refused electrical CV. The remaining 67 patients underwent electrical CV which was successful in 56 of them. Cerebral embolism occurred 24 hours after CV in one patient who did not receive anticoagulation. Repeat TEE soon after embolism showed absence of thrombus or spontaneous echo contrast, but the presence of low flow velocity in the left atrial appendage.In patients in AF candidates for CV, exclusion of thrombi or prethrombotic conditions by TEE does not exclude the risk of thromboembolic events and the need for anticoagulant therapy. Left atrial appendage function can be stunned or impaired immediately after CV, favouring a thrombogenic milieu and subsequent embolic events. Therapeutic anticoagulation at the time of as well as after cardioversion is actually recommended.

We studied 142 patients (121 males, 21 females) survivors of a first non complicated acute myocardial infarction (AMI) treated with thrombolytic therapy between March 1988 and December 1989. Dipyridamole echocardiography test (DET, 67 patients) and exercise electrocardiography test (EET, 104 patients) were performed to assess sensitivity and specificity in identifying patients at risk for an unfavorable clinical outcome and subsequent cardiac events: 67 patients underwent coronary arteriography within 4 weeks after AMI. DET positivity was related to the detection of a new transient asynergy of contraction either in infarct area or in remote zones. The mean follow-up period was 12 months (range 4-20). Clinical follow-up end-points of the study included death, re-AMI, angina. Sensitivity and specificity of EET and DET were 75 and 68%, 53 and 71% respectively. If EET plus DET were considered, sensitivity was 81% and specificity 60%. The fairly good DET sensitivity and specificity could be partially explained by some stunned myocardium exhibiting prolonged contractile dysfunction despite myocardial reperfusion. EET sensitivity and specificity is comparable to previous observations in AMI not treated with thrombolytic therapy. DET seems to be a useful and safe test in prognostic evaluation of asymptomatic patients after thrombolysed AMI, but its value is improved in association with EET.

Static lung volumes, flow volume curve in air and in a helium-oxygen mixture, PaO2 and pulmonary vascular pressures were measured in 16 patients 2 weeks after uncomplicated acute myocardial infarction and repeated 2 h after furosemide 40 mg i.v. administration. The patients with wedge pressure (WP) greater than 18 mm Hg had significantly lower values of FEV1, FEV1/VC%, MEF40 and MEF 25 in comparison with the patients with WE less than 18 mm Hg. A negative correlation was found between both PAP and WP and MEF25 values (p less than 0.001). After furosemide respiratory function tests improved only in patients with a good hemodynamic response to the drug. PaO2 did not change significantly. Airflow response to helium seemed to be a useful test for determining the site of major bronchial compression.

The extent to which patients with low peak serum creatine kinase (CK) at their first myocardial infarction differ from patients with high CK levels in terms of risk for subsequent ischaemic events was investigated in 266 patients who survived the first 48 h from the onset of infarction. All patients were followed up for one year. Four groups were formed based on peak CK less than or equal to 200, 201-400, 401-800 and greater than 800 IU l-1. During follow-up the incidence of mortality was 15% (N = 39), non-fatal re-infarction 9% (N = 23), and angina 53% (N = 140). Hospital mortality was significantly higher (P less than 0.02) in the highest CK-group (16%), but the incidence of non-fatal re-infarction, angina pectoris and late mortality was similar in the four groups. In hospital survivors, ischaemic ST-changes during pre-discharge symptom limited bicycle stress test and multiple vessel disease were equally distributed in all four groups. We conclude that while hospital mortality is directly related to peak CK, there is no relationship between peak CK and late mortality, non-fatal re-infarctions, or recurrent angina. Accordingly, diagnostic and therapeutic procedures in the individual patients are not influenced by the amount of serum CK released during acute infarction.