Anterior transmural myocardial infarction: controlled randomized studies.
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Biomedical subjects
Publications and source records attributed to D H Spodick.
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In 20 consecutive patients with echocardiographic pericardial effusions and no pulsus paradoxus or other signs of cardiac embarrassment the left ventricular ejection time fell (delta LVET) during inspiration by 18.3 +/- 2.47 (SE) ms, greatly exceeding mean inspiratory delta LVET in normal subjects (7.0 ms). Median and mode delta LVET were each 15.0 ms, with delta LVET less than 10 ms and more than 25 ms in only 1 patient each. With a single exception, the magnitude of the abnormal delta LVET was least in patients with minimal to small effusions. Ejection time indices were normal during expiration and low during inspiration, indicating diminished stroke volume during inspiration only. Thus, even without clinical and echocardiographic signs of cardiac compression, the presence of pericardial fluid clearly exaggerated respiratory effects on left ventricular function but not to the degree characteristic of overtly compressing (tamponading) fluid. The consistent exaggeration of delta LVET during even small pericardial effusions is thus of physiologic interest and may be of diagnostic value.
The peak derivative of the ear densitograph displacement pulse was monitored on 12 patients undergoing routine coronary angiography and left ventricular angiography. Simultaneous recording of cardiac output, heart rate, systolic time intervals, and ear densitogram were obtained throughout the progression from before angiographic injections to postcoronary angiography to after left ventricular angiography. The peak derivative of the ear densitogram (PD) consistently tracked mean systolic ejection rate, and changes in PD showed good correlation with changes in ejection rate (r=.749, p less than 0.0001). The PD of the ear densitogram appears to be a reliable noninvasive tool for tracking left ventricular function during hemodynamic and other challenges.
Owing to the interaction between the left ventricle and the arterial system, pulse contour during ejection is significantly affected by changes in peripheral resistance. Quantitative description of the pulse configuration as a function of peripheral resistance involves invasive investigation of complex frequency and impedance spectra. The ear densitogram noninvasively yields a pulse wave shown to closely track changes in the central arterial pulse; in this investigation, its decreasing systolic slope responded to changes in the peripheral resistance like those in the central pulse and in arterial models. The decreasing slope of the ear densitogram pulse (RNAD) can reliably track changes in peripheral resistance.
We report a rare electrocardiographic finding occurring in previously undescribed circumstances in which a 61-year-old man undergoing exercise testing developed striking ST segment elevation on the ECG characterized by electrical alternans of the ST segments. The significance of electrical alternans is briefly discussed in the light of this event.
Certain behavioral characteristics of physicians have traditionally lead to erroneous therapeutic observations. Appropriately designed clinical trials overcome behavioral pitfalls to insure a scientific (hence, ethical) result.
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Bedside estimation of the rate of rise of the carotid pulse is a standard clinical observation whose reliability has not been determined. To ascertain interobserver agreement (primary objective) and compare the velocity of rise of the carotid displacement (not pressure) pulse (supplementary objective), three blinded observers evaluated, ranked and palpated the velocity of rise of carotid pulse as "unremarkable," "slow" or "rapid" in 20 consecutive patients. The relative rate of rise of the recorded carotid pulse was represented by the angle between baseline and the initial carotid peak at a standard paper speed of 100 mm/s. Chi-square analyses yielded no significant interobserver agreements (probability [p] 0.22 to 0.51). There was also no correlation of observers' ranking of rise of carotid pulse with the ranking from independent measurement of the recorded pulse rise velocity (p = 0.10 to 0.99). Observer agreement was unanimous only four times and even in these instances was consistent with the recorded carotid pulse rise velocity only once. The results suggest that unbiased observers cannot reliably discriminate slow from "normal" velocity of rise of carotid pulse.
Randomized controlled trials are increasingly accepted in principle but not always in practice, particularly for surgical therapies. Successful surgical randomized controlled trials demonstrate their feasibility, and reports of uncontrolled surgical trials now commonly bear a statement that a definitive answer requires a controlled trial. Scientifically, the randomized controlled trial is the most powerful way to determine a result ascribable only to the trial treatment. Although randomized controlled trials can be imperfect or improperly conducted, they are designed to circumvent biased behavior by investigators. With candor in informed consent, the equal chance not to get a trial treatment makes the randomized controlled trial the most ethical design. Thus, scientific, behavioral, and ethical cases support the randomized controlled trial as the optimal method for investigation of nearly all therapeutic innovations and as a requirement for publication.
The outcome of 50 consecutive modified predischarge exercise tests after acute myocardial infarction was predicted by three independent observers on the basis of ST segment displacement in the resting pretest 12 lead electrocardiograms. The mean predictive accuracy for the three observers was 82% for a positive test defined as additional ST segment depression or elevation greater than or equal to 0.1 mV, and rose to 94% for a positive test defined as additional ST segment depression greater than or equal to 0.1 mV alone. For the majority of patients, the test result was already apparent in the resting 12 lead electrocardiogram.
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The effect of oral propranolol on left ventricular performance during early upright exercise was evaluated by ear densitography in patients with arteriographic coronary artery disease (CAD). Measurements of systolic time intervals differentiated 10 unmedicated patients with CAD (group 1) and 15 patients with CAD taking propranolol (group 3). The patients in group 3 had less shortening of preejection period at 1 minute and 4 minutes of exercise than group 1 patients (p less than 0.001 and p less than 0.005, respectively), with propranolol appearing to prevent the abnormal shortening of preejection period seen in the unmedicated group. Group 3 patients, in contrast to group 1 patients, showed reduction of heart rate and heart rate-blood pressure product both at rest and during exercise. Furthermore, PEP/LVET and percentage change in PEP/LVET from control responses were similar to those of subjects free of CAD (group 2). These results indicate that propranolol effects a favorable change in LV performance by postponing early exhaustion of cardiac reserve, despite significant CAD. There was relatively large overlap in percentage change in PEP/LVET from control between group 2 and group 3 in contrast to the clear separation among unmedicated patients. Thus, the excellent diagnostic accuracy of systolic time intervals recorded during exercise is greatly reduced by beta-adrenoceptor blockade.