Optimal stage duration in dobutamine stress echocardiography.

OBJECTIVES: This study attempted to determine the benefit of a 5-min dobutamine stress echocardiographic stage versus a 3-min stage in a canine model. BACKGROUND: Dobutamine stress echocardiography, as currently performed, uses a variety of different protocols. Among the many aspects of dobutamine stress echocardiographic protocols that vary is stage duration. Because dobutamine has specific pharmacodynamics, it is possible that stages of different durations may have different cardiovascular effects. METHODS: Paired dobutamine stress echocardiograms were obtained in 10 open chest instrumented dogs. The stage duration for the initial dobutamine stress echocardiogram was randomly allocated to either 3 or 5 min, and all hemodynamic and echocardiographic variables were allowed to return to baseline before the second dobutamine stress echocardiogram was obtained using the alternative stage duration. At each stage, heart rate, systolic blood pressure, coronary flow, myocardial wall thickness and left ventricular cavity area were recorded. Cavity obliteration, hypotension, ventricular tachycardia or a maximal dose of 40 micrograms/kg body weight per min served as the dobutamine stress echocardiographic end point. RESULTS: At baseline, no difference was detected between the 3- or 5-min protocols for heart rate, systolic blood pressure, rate-pressure product, coronary blood flow, wall thickness or percent area change. Heart rate, systolic blood pressure and coronary flow increased more by the 10-micrograms/kg per min dose with the 5-min protocol than with the 3-min protocol. The dobutamine stress echocardiographic end points were achieved at a lower dobutamine dose (15.0 +/- 4.1 vs. 11.0 +/- 2.1 micrograms/kg per min [mean +/- SD], p = 0.01) with the longer stage duration. CONCLUSIONS: In this canine model, a longer stage produced a greater hemodynamic effect at a lower peak dose. Thus, extending stage duration in clinical dobutamine stress echocardiography may achieve equivalent physiologic stress at lower doses and contribute to the optimization of dobutamine stress echocardiographic protocols.

Benefit of late coronary reperfusion on ventricular morphology and function after myocardial infarction.

OBJECTIVES: This study was designed to examine the relation between the timing and adequacy of perfusion of the infarct bed and changes in ventricular size and the extent of abnormal wall motion after acute myocardial infarction. METHODS: A validated echocardiographic mapping technique was used to measure the left ventricular endocardial surface area index and the extent of abnormal wall motion over a 3-month period in 91 patients who had either 1) no anterograde or collateral flow to the infarct bed (n = 14), 2) only collateral flow to the infarct bed (n = 18), 3) restoration of anterograde flow to the infarct bed within hours of chest pain (early [n = 43]), or 4) restoration of anterograde flow to the infarct bed within a mean of 5 days after acute myocardial infarction (late [n = 16]). RESULTS: Over the follow-up period, a progressive and significant increase in endocardial surface area index was observed only in the group of patients without anterograde or collateral flow to the infarct bed (entry 64 +/- 3.4 cm2/m2 vs. 3 months 75.9 +/- 6.4 cm2/m2, p < 0.005). In contrast, a progressive reduction in the extent of abnormal wall motion was evident in the group of patients in whom anterograde flow to the infarct bed was restored within hours (entry 26.7 +/- 2.5 cm2 vs. 3 months 11.8 +/- 2.9 cm2, p < 0.001) or days (entry 22.1 +/- 3.6 cm2 vs. 3 months 11.8 +/- 3.3 cm2, p < 0.001) of coronary occlusion. Multiple stepwise linear regression analysis confirmed that by 3 months, 1) ventricular size was independently related to endocardial surface area index and abnormal wall motion at entry (p < 0.0001) and to the change in abnormal wall motion over the follow-up period (p < 0.0001), and 2) the change in abnormal wall motion was related to the presence of anterograde flow to the infarct bed (p < 0.0001) independent of the timing of reperfusion, infarct site or the extent of abnormal wall motion on admission. CONCLUSIONS: After myocardial infarction, the process of ventricular remodeling is influenced by changes in the extent of abnormal wall motion, which in turn are related to the adequacy rather than the timing of perfusion of the infarct bed.

New perspectives in the assessment of cardiac chamber dimensions during development and adulthood.

The use of body surface area to assess the normalcy of cardiac dimensions has several limitations. To determine whether cardiac dimensions can be assessed by other indexes of body size and growth, this study evaluated the relations between cardiac dimensions assessed by two-dimensional echocardiography and age, height, weight and body surface area. The study group included 268 normal persons aged 6 days to 76 years of age. The dimensions examined included the aortic anulus, left atrium and left ventricular end-diastolic diameter, each measured in the parasternal long-axis plane, and left ventricular length measured from the apical two-chamber view. The analysis confirmed that the heart and great vessels grow in unison and at a predictable rate after birth, reaching 50% of their adult dimensions at birth, 75% by 5 years and 90% by 12 years. Although each cardiac dimension related linearly with height (aortic anulus, r = 0.96; left atrium, r = 0.91; left ventricular diameter, r = 0.94; left ventricular length, r = 0.93), the relations among age, weight and body surface area were best expressed by quadratic equations. Multiple regression confirmed that after adjustment for height, other indexes including age, gender, weight and body surface area had no independent effect on the prediction of each dimension. Therefore, because height is a nonderived variable that relates linearly with cardiac dimensions independent of age, it offers a simple yet accurate means of assessing the normalcy of cardiac dimensions in children and adults.

Whole blood aggregation, thromboxane release and the lyso derivative of platelet activating factor in myocardial infarction and unstable angina.

To investigate the pathophysiology of intracoronary thrombus formation we measured whole blood aggregation in response to ADP, platelet activating factor (PAF) and collagen, along with thromboxane B2 (TXB2) production during collagen induced aggregation, plasma TXB2 and plasma levels of lyso-PAF, in 38 subjects with and without ischaemic heart disease (12 with acute myocardial infarction, 9 with prolonged ischaemic chest pain without infarction and 17 normals). Lyso-PAF was measured, after in vitro acetylation to active PAF, by bioassay using 14C-serotonin labelled rabbit platelets. TXB2 was measured by radioimmunoassay. Plasma TXB2 was elevated at presentation only in patients with myocardial infarction (p less than 0.01). While impedance aggregation was similar in the three groups, aggregation to collagen resulted in greater release of TXB2 in subjects with myocardial infarction (p less than 0.01), an abnormality persisting 2-4 months later. Plasma lyso-PAF levels were significantly depressed throughout the first week in subjects with infarction (p less than 0.002), but after 2 to 4 months the level was greater than in normal subjects (p less than 0.001), changes presently unexplained. It is possible that the disorder of platelet function preceded and predisposed to coronary thrombosis. The findings strengthen the grounds for aspirin therapy in acute myocardial infarction.

Prognostic significance of an early rise to peak creatine kinase after acute myocardial infarction.

Because an early rise to peak creatine kinase (CK) is regarded as a noninvasive marker of early coronary reperfusion, the short- and long-term significance of this phenomenon was studied. In a series of consecutive patients admitted between 1974 and 1976 with acute myocardial infarction (AMI), 2 hourly CK estimations were performed. Complete CK curves were obtained in 102 patients, all of whom have been followed for 10 years. Without reference to their clinical course or follow-up, patients were divided into those with CK curves peaking less than or equal to 15 hours (mean 11 hours; n = 41) and those with curves peaking greater than 15 hours (mean 21 hours; n = 61). There were no differences in age, Norris index, location of AMI or past history of coronary artery disease between the groups; however, the mean peak CK was higher in the late peak group (p less than 0.05) and there were more non-Q-wave infarcts in the early peak group (p less than 0.01). In the first 9 months of follow-up there were fewer cardiac deaths in the early peak group (5 vs 13%), but this difference was not significant, and at 12 months the survival curves crossed. At 10 years, survival was 42% in the early peak group and 65% in the late peak group (p less than 0.05). Cox regression analysis showed that early peaking of the CK curve was an independent marker for cardiac death overall (relative risk 2.3, p less than 0.02). In 1-year survivors the relative risk increased to 3.8 (p less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hydration on cavity obliteration during dobutamine stress echocardiography.

The purpose of this study was to determine whether it is possible to prevent or delay the onset of midventricular cavity obliteration during a dobutamine stress test with standard hydration. Left ventricular (LV) intracavitary obstruction has been reported as the mechanism for hypotension seen in approximately 20% of patients undergoing dobutamine stress echocardiography. In addition, it has been proposed that administration of a normal saline bolus prior to dobutamine infusion may avert the dynamic ventricular obstruction. We performed a standard graded dobutamine stress echocardiogram before and after fluid loading with 10 ml/kg of normal saline in 10 mongrel dogs. Measurements were made of left atrial pressure, aortic pressure, and the area of the LV cavity at the papillary muscle level throughout each infusion. Although hydration produced an increase in baseline left atrial pressure (5.7 +/- 3.2 to 8.1 +/- 2.7 mmHg, p < 0.01) and systolic blood pressure (128 +/- 18 to 139 +/- 22 mmHg, p = 0.03), there was no significant change in pre-dobutamine heart rate or systolic area. With dobutamine infusion, there was a similar change in heart rate, systolic blood pressure, diastolic area, and systolic area (SA) at each dose of dobutamine regardless of hydration status. In addition, the dose at which cavity obliteration occurred was not altered by hydration (p = NS). Although all dogs developed cavity obliteration (SA < 1.0 cm2) with dobutamine infusion, none experienced hypotension. In this canine model, cavity obliteration does not lead to systemic hypotension and cannot be prevented or delayed by volume loading.

Reduced risk of death at 28 days in patients taking a beta blocker before admission to hospital with myocardial infarction.

OBJECTIVE: To see whether patients taking an oral beta blocker at the time of admission to hospital with myocardial infarction have a reduced risk of death at 28 days. DESIGN: Retrospective analysis of data collected on patients admitted over four years. SETTING: Community based study. PATIENTS: 2430 Consecutive patients living in the Perth statistical division admitted to hospital with myocardial infarction during 1984-7. MAIN OUTCOME MEASURE: Survival at 28 days among patients taking a beta blocker at onset of myocardial infarction. RESULTS: Patients were grouped into those who were and were not taking a beta blocker at the time of admission. Though patients taking a beta blocker were older and more likely to have a history of myocardial infarction, angina, or hypertension, the overall mortality at 28 days was similar in the two groups. A logistic regression model used to adjust for factors predictive of cardiac death at 28 days confirmed that patients taking a beta blocker at the time of admission had a significantly reduced risk of death (relative risk 0.50; 95% confidence interval 0.34 to 0.76). Though the incidence of fatal ventricular fibrillation was similar in the two groups, mean peak creatine kinase activity was significantly lower in the beta blocker group. CONCLUSIONS: These data support the value of long term use of beta blockers in patients at risk of myocardial infarction. They suggest that patients taking these agents before admission to hospital with myocardial infarction have a significant survival advantage at 28 days, which may be due to a reduction in infarct size.

The benefits of beta-blockade at the time of myocardial infarction.

Data from the World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease (WHO MONICA) project, collected in Perth, are described. Patients taking a beta-blocker at the time of onset of myocardial infarction are a high-risk group, but univariate analysis of the data showed that the overall survival of patients on beta-blockers at 28 days was the same as for those not taking beta-blockers. A multiple logistic regression model analysis showed that the patients treated with beta-blockers had a survival advantage at 28 days, with a relative risk of death of 0.5. The mechanism of benefit is unclear. It does not appear to be an anti-arrhythmic effect, because beta-blockers did not affect survival in the first 24 h following a myocardial infarction, nor did they affect ventricular fibrillation. The effect may be due to a reduction in myocardial necrosis. Furthermore, an analysis of the incidence of coronary disease and type of drugs prescribed in Perth has indicated that beta-blockers may be contributing to a decrease in mortality due to coronary events.

The effect of late patency of the infarct-related coronary artery on left ventricular morphology and regional function after thrombolysis.

The use of early coronary angiography to assess the benefits of coronary patency on left ventricular size and function fails to account for subsequent reocclusion or spontaneous reperfusion. To investigate the relationship between late vessel patency and changes in left ventricular structure and function after thrombolysis, echocardiography was performed within 48 hours and at 6 to 12 weeks in 30 patients treated with intravenous thrombolysis. Left ventricular endocardial surface area index (ESAj; cm2/m2) and extent of abnormal wall motion were quantitated in those with a patent (n = 20) and those with an occluded (n = 10) infarct-related artery on coronary angiography performed 8 +/- 6 days after thrombolysis. Mean ESAi increased from (53 +/- 7 to 61 +/- 10 cm2/m2; p less than 0.02) in the occluded group during the follow-up period but remained unchanged (60 +/- 11 to 62 +/- 11 cm2/m2; p = NS) in the patient group. Mean percentage of abnormal wall motion decreased in the patent group (27 +/- 16% to 18 +/- 16%; p less than 0.01), whereas no significant change was noted in the occluded group (20 +/- 13% to 23 +/- 17%; p = NS). Thus coronary patency at days after thrombolysis is associated with both improvement in regional left ventricular function and attenuated left ventricular dilatation.

Three-dimensional intravascular ultrasound assessment of plaque volume after successful atherectomy.

The primary purpose of directional coronary atherectomy is the removal of intraluminal plaque. Angiography allows assessment of residual lumen narrowing but is limited in the assessment of residual plaque burden. Intravascular ultrasound has proven useful in assessing plaque size, but current use has been limited to a single, representative cross-sectional image rather than an evaluation of the entire plaque volume. To determine the volume of residual plaque after angiographically successful directional coronary atherectomy ( < or = 20% residual stenosis), we performed intravascular ultrasound in 19 patients before and after atherectomy. Only coronary lesions optimal for three-dimensional analysis (a single, discrete stenosis in a nontortuous, noncalcified native coronary artery) were selected. A 2.9F sheath-design intravascular ultrasound catheter with a motorized pullback device was used in all patients. The cross-sectional area of the artery (defined by the medial-adventitia border), the lumen, and the plaque were measured at 1 mm intervals over a 15 to 20 mm segment, which included the target lesion and a proximal reference segment (n = 362 cross-sections), before and after atherectomy. The volumes of the artery, vessel lumen, or plaque were calculated with a modified Simpson's equation and compared with standard area measurements at the point of maximal stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)