Discontinuation of chronic diuretic therapy in stable congestive heart failure secondary to coronary artery disease or to idiopathic dilated cardiomyopathy.

To assess the feasibility of diuretic discontinuation in patients with stable congestive heart failure (CHF) and to identify risk factors for subsequent development of congestion, a prospective, 12-week clinical trial of unmasked diuretic withdrawal was conducted with continuation of background CHF therapy and double-blind randomization to placebo or lisinopril. Forty-one patients with a history of CHF and continuous diuretic use for > or = 3 months had all diuretic therapy discontinued, and therapy with lisinopril 5 mg (target 20 mg)/day (n = 20) or placebo (n = 21) begun the next day. A diuretic was restarted if new or worsening CHF symptoms and signs developed. Twelve patients (29%) did not require diuretic reinitiation at any time during follow-up, whereas 29 (71%) restarted diuretic therapy after a median of 15 days (range 2 to 42). Fourteen patients taking lisinopril and 15 taking placebo required diuretic drugs (p = NS). The baseline daily furosemide dose of > 40 mg, a left ventricular ejection fraction < or = 0.27, and history of systemic hypertension were independently predictive of early diuretic reinitiation by Cox proportional-hazards analysis. The probability of remaining diuretic-free after 6 weeks was 71% if none of these criteria were present. This trial demonstrates the feasibility of discontinuing diuretic drugs in certain patients with stable CHF and predicts those patients likely to require reinitiation of therapy. Diuretic withdrawal may be warranted when the furosemide dose is < or = 40 mg/day, left ventricular ejection fraction is > 0.27 and when no history of systemic hypertension is present.

Comparison of adenosine echocardiography, with and without isometric handgrip, to exercise echocardiography in the detection of ischemia in patients with coronary artery disease.

This study was undertaken to evaluate whether adenosine echocardiography is comparable to exercise echocardiography in the detection of ischemia in patients with suspected coronary artery disease and to assess whether the addition of handgrip exercise to adenosine enhances the induction of ischemia in these patients. Accordingly, 67 patients with suspected or known coronary artery disease referred for exercise testing underwent adenosine, adenosine with handgrip, and post-treadmill exercise echocardiography. A maximal adenosine infusion dose of 170 micrograms/kg/min was used. Images at baseline and during each of the three stress modalities were digitized in a quad-screen format, randomized, and blinded as to the stage and mode of intervention for nonbiased interpretation. An ischemic response was defined as a new or worsening wall motion abnormality. Ischemia was detected by exercise echocardiography (n = 20) more often than by adenosine echocardiography alone (n = 11; p = 0.039) but similarly to adenosine plus handgrip (n = 16; difference not significant). Exact agreement in individual response between exercise adenosine echocardiography was seen in 51 (80%) of 64 patients and increased to 88% between exercise and adenosine plus handgrip. In the patients who underwent angiography (n = 45), the sensitivity for coronary artery disease (n = 33) was 87% for adenosine, 91% for adenosine plus handgrip, and 93% for exercise echocardiography. The respective sensitivities decreased to 64%, 81%, and 89% in patients without previous myocardial infarction. Specificity was 91% for adenosine with or without handgrip and 82% for exercise echocardiography. Image quality during adenosine with and without handgrip was superior to that during exercise (p < 0.01). Thus in patients with coronary artery disease able to exercise, exercise echocardiography induces ischemia more frequently than does adenosine echocardiography alone. The addition of handgrip exercise to adenosine infusion enhances the detection of ischemia without reducing specificity or image quality and is recommended when adenosine echocardiography is used as a pharmacologic stress test.

Use of a rapid assay of subforms of creatine kinase MB to diagnose or rule out acute myocardial infarction.

BACKGROUND: Ruling out myocardial infarction in patients coming to the emergency room with chest pain is hindered by the lack of a specific early diagnostic marker. Less than 30 percent of patients admitted to coronary care units have infarction, resulting in substantial unnecessary expenditures. We developed a rapid assay of the subforms of creatine kinase MB (CK-MB) and prospectively analyzed its sensitivity and specificity in diagnosing myocardial infarction in the first six hours after the onset of chest pain. METHODS: In 1110 consecutive patients who came to the emergency room with chest pain, blood samples were collected every 30 to 60 minutes until at least 6 hours after the onset of symptoms; in patients who were then admitted to the hospital, samples were collected every 4 hours for up to 48 hours. The samples were analyzed for CK-MB subforms, and the diagnosis of myocardial infarction was confirmed by conventional CK-MB analysis. RESULTS: Of the 1110 patients evaluated, 121 had myocardial infarction. The sensitivity of the assay of CK-MB subforms to detect myocardial infarction in the first six hours after the onset of symptoms was 95.7 per cent, as compared with only 48 percent for the conventional CK-MB assay; the specificity was 93.9 percent among patients hospitalized without myocardial infarction and 96.2 percent among those sent home. Among the patients with myocardial infarction, definitive results of the subform assay were available a mean (+/- SD) of 1.22 +/- 1.17 hours after their arrival in the emergency room. CONCLUSIONS: The assay of CK-MB subforms reliably detected myocardial infarction within the first six hours after the onset of symptoms, and its use could reduce admission to the coronary care unit by 50 to 70 percent, thereby reducing costs.