Predicting ejection fraction after myocardial infarction.
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Biomedical subjects
Publications and source records attributed to M J Zema.
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Electrocardiographic tall R waves in the right precordial leads may be present in patients with posterior myocardial infarction, right ventricular hypertrophy, various conduction disturbances, and some forms of cardiomyopathy and in clinically otherwise normal subjects with prominent anterior electromotive forces. Clinical uncertainty most often arises in distinguishing possible prior posterolateral myocardial infarction (PMI) from the unusual normal variant (PAF). The ECGs and VCGs of 15 subjects with posterolateral infarction were compared with tracings from 12 subjects with no evidence of cardiac disease, all individuals demonstrating tall R waves (R/S greater than 1.0 in V1 and/or V2) in the right precordial leads on surface ECG. By standard ECG, the infarction group was characterized by taller T waves in leads V1 and V2, shorter T waves in V6, greater T2-T6 index, and a more negative two variable function as described by Nestico. By VCG, the infarction group was characterized by a more anteriorly oriented T loop, more leftward maximal frontal plane QRS vector and a lower calculated -45 degrees/ab, as described by Suzuki. An algorithm was proposed that permitted proper classification (PAF vs. PMI) based on ECG criteria in 75% of subjects with 90% accuracy. This compared favorably with performance of the Frank vectorcardiogram, including using more recently proposed criteria. Routine use of the VCG, therefore, in this clinical setting may no longer be justified.
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The tendency of oral diltiazem (a calcium entry blocking agent and a negative inotrope) to induce or exacerbate congestive heart failure when used for the long term management of myocardial ischaemia in patients with poor left ventricular function has not been investigated before. Twenty two patients (aged 42-73 years) with pretreatment left ventricular ejection fraction ranging from 0.11 to 0.39 were given open label oral diltiazem (120-360 mg/24 h (mean 254 mg)) for two weeks to 16 months (mean 7.5 months, median 6.2 months). There was a weight change of greater than 3 lb (1.35 kg) in nine patients--five gained weight and four lost it. Diltiazem treatment did not alter the mean (SD) cardiothoracic ratio on chest x ray (0.47 (0.06) before vs 0.48 (0.05) after) or the left ventricular ejection fraction at rest (0.28 (0.09) before vs 0.26 (0.08) after). Diltiazem was discontinued in one patient because of symptoms indicative of worsening congestive heart failure. No patient required admission to hospital for treatment of symptoms resulting from further left ventricular decompensation. Diltiazem was discontinued in six other patients for other reasons. Long term administration of oral diltiazem was not regularly associated with a deterioration in clinical, radiographic, or radionuclide ventriculographic estimates of left ventricular function, even in patients with poor baseline left ventricular systolic performance.
Abundant experimental and clinical evidence now suggests that the presence or absence of Q waves on surface electrocardiography does not permit distinction between pathologic transmural and subendocardial myocardial infarction. It has been recommended, therefore, that use of certain electrocardiographic descriptors of myocardial infarction be avoided. One hundred fourteen consecutive patients with first myocardial infarction were studied. The lack of development of Q waves accompanying acute myocardial infarction delineated a group of patients with low in-hospital mortality. Left ventricular ejection fraction was less after Q wave (0.48 +/- 0.16) than after non-Q wave (0.67 +/- 0.10) infarction (p less than 0.0001). Left ventricular end-diastolic pressure was greater after Q wave (16.1 +/- 5.9 mm Hg) than after non-Q wave (11.7 +/- 2.7 mm Hg) infarction (p less than 0.02). Fixed thallium perfusion scintigraphic defects were more common in survivors of Q wave (98 percent [41 of 42]) than in survivors of non-Q wave (64 percent [seven of 11]) infarction (p less than 0.002). Objectively demonstrable myocardial ischemia was more common after non-Q wave (68 percent [13 of 19]) than after Q wave (32 percent [16 of 50]) infarction (p less than 0.01). The incidence of late cardiac events (sudden death plus reinfarction) did not differ after Q wave or non-Q wave infarction. Q wave, S-T segment, and T wave myocardial infarctions differ physiologically, clinically, and prognostically. It is of little consequence to the clinician managing patients whether such useful electrocardiographic descriptors also accurately define groups that differ anatomically with regard to the thickness of the injured myocardial wall.
One hundred survivors of first myocardial infarction were studied prior to hospital discharge by 24 hour ambulatory electrocardiography as well as radionuclide ventriculography. The bedside Valsalva maneuver, with simple sphygmomanometric determination of arterial pressure response, was performed 6 weeks post infarction and patients were followed for a mean of 22 months. The arterial pressure response pattern provided a semiquantitative estimate of resting left ventricular systolic function when related to the radionuclide ejection fraction (SIN, 0.56 +/- 0.13; ABO, 0.43 +/- 0.18; SQW, 0.16 +/- 0.06) (P less than 0.02). Abnormal Valsalva responses (ABO and SQW) were found more commonly in patients with diminished left ventricular systolic function and high grade ventricular arrhythmias. The SQW response pattern was highly predictive of future sudden cardiac death. The bedside Valsalva maneuver, performed 2-4 weeks after hospital discharge, upon the ambulatory patient is a simple, safe, inexpensive and uniformly applicable method which may serve as the basis for a strategy with which to approach the post-infarction patient regarding risk stratification and further clinical management.
Electrocardiographic tall R waves in the right precordial leads may be present in patients with posterior wall myocardial infarction, right ventricular hypertrophy, various conduction disturbances, some forms of cardiomyopathy, and in clinically otherwise normal subjects with prominent anterior forces. Since clinical uncertainty most often arises in distinguishing possible prior posterior myocardial infarction from the unusual normal variant, we compared VCGs and ECGs in 19 subjects with posterior infarction with tracings from 11 subjects with no evidence of cardiac disease who had prominent anterior forces on routine examination. By VCG, the infarction group was characterized by smaller maximum posterior voltage in the horizontal plane, more anteriorly oriented T loop direction, more prolonged anterior QRS forces, more leftward frontal plane QRS maximum vector, and associated evidence of diaphragmatic infarction. By standard ECG, the infarction group was characterized by isoelectric or upright T waves in precordial lead V1, a more leftward frontal plane axis, and associated diaphragmatic infarction. Criteria for distinguishing between posterior wall myocardial infarction and prominent anterior forces in otherwise clinically normal subjects are suggested. These require prospective validation in an independent test population.
Despite widespread marketing of a controlled-released preparation of disopyramide phosphate (Norpace-CR, G. D. Searle), literature demonstrating its efficacy in maintaining uniform serum drug levels over a 12-h dosing interval is derived from only normal healthy volunteers. Twenty patients with cardiac arrhythmias (ages 37-80 years) were administered 400-800 mg/24 h (5.1-10.5 mg/kg/day) of controlled-release disopyramide in two equally divided doses on a q. 12 h. schedule. After achievement of steady-state equilibrium drug concentration, disopyramide levels were determined by high-pressure liquid chromatography on sera obtained from blood samples drawn 2, 7, and 11 h after an oral dose. Mean maximal and minimal disopyramide serum concentrations were 3.2 +/- 1.0 and 2.5 +/- 0.9 microgram/ml, respectively. Adverse drug effects occurred in nine (45%) subjects, necessitating discontinuation of the preparation in five patients (25%). These data demonstrate that in a population of patients with cardiac arrhythmias q. 12 h. dosing with a controlled-release disopyramide phosphate preparation is associated with an acceptable variation between maximal and minimal serum disopyramide concentrations, and is tolerated by the majority of subjects. The preparation should, therefore, offer greater patient convenience and compliance without sacrificing antiarrhythmic efficacy.
Thirty-seven patients with dyspnea, clinical chronic obstructive pulmonary disease and abnormal pulmonary function tests demonstrating an obstructive airways pattern underwent six-foot posteroanterior chest radiography, radionuclide ventriculography and sphygmomanometer-monitored arterial pressure response during a bedside Valsalva maneuver. Patients could be separated into three groups (square wave, absent overshoot, sinusoidal) on the basis of their Valsalva response which corresponded to left ventricular ejection fractions on radionuclide ventriculography of 0.19 +/- 0.05, 0.42 +/- 0.20, 0.64 +/- 0.13 (p less than 0.005 for differences between all group means). Pulmonary function test results and a detailed patient history could not accurately separate patients with primary pulmonary dyspnea from those with concomitant left ventricular dysfunction (ejection fraction less than 0.50). In this population of patients, however, both the sensitivity (88 percent) and predictive value (88 percent) for the presence of left ventricular dysfunction of an abnormal (square wave or absent overshoot) systolic arterial pressure response during Valsalva maneuver were high. Thus, in dyspneic subjects with clinical evidence of chronic obstructive airways disease, concomitant left ventricular dysfunction can be accurately diagnosed using the simple Valsalva maneuver without sophisticated equipment or highly trained personnel.
The bedside sphygmomanometric determination of the arterial pressure response during the Valsalva maneuver was incorporated into the routine physical examination of ambulatory subjects. Four distinct Valsalva responses were noted: ultrasinusoidal, sinusoidal, absent overshoot, and square wave. The absent overshoot response was further divided into positional and constant types--the latter consistently exhibiting this response regardless of body position. Correlation with resting left ventricular ejection fraction was obtained by radionuclide cineangiography in 200 patients, of whom 81 had left ventricular systolic dysfunction (ejection fraction less than 0.50). Significant differences in the mean left ventricular ejection fraction were found in subjects with an ultrasinusoidal response (0.65 +/- 0.11), sinusoidal response (0.55 +/- 0.15), constant absent overshoot response (0.37 +/- 0.18), and square wave response (0.16 +/- 0.04) to Valsalva maneuver. The sensitivity of an abnormal Valsalva response (absent overshoot or square wave responses) for the bedside detection of left ventricular systolic dysfunction was 69 percent, and the predictive value of an ultrasinusoidal Valsalva response for normal ejection fraction was 93 percent. It is concluded that the high predictive accuracy of the Valsalva maneuver makes this simple bedside technique a valuable method for assessing resting left ventricular function.
Despite widespread marketing of a sustained release preparation of procainamide hydrochloride (PROCAN-SR, Parke-Davis), published literature demonstrating its efficacy in maintaining uniform serum drug levels over a 6-hour dosing interval is derived from only normal healthy volunteers. Thirty-three patients with ischemic heart disease, ages 30-88 years, were administered 1-4g/24 hours (mean dose 34 mg/kg/day) of PROCAN-SR in 4 equally divided doses on a Q6H schedule. After achievement of steady-state equilibrium drug concentration, procainamide and N-acetylprocainamide levels were determined by high-performance liquid chromatography on sera obtained from blood samples drawn 2, 3.5 and 5 hours after an oral dose. Mean maximal procainamide and N-acetylprocainamide serum concentrations were 4.6 +/- 1.8 microgram/ml and 4.2 +/- 2.1 micrograms/ml respectively. Mean minimal concentrations were 3.5 +/- 1.7 microgram/ml and 3.6 +/- 2.0 micrograms/ml respectively. The mean change in drug concentration was small (1.1 microgram/ml procainamide and 0.6 microgram/ml N-acetylprocainamide) with procainamide and N-acetylprocainamide concentrations varying only by 27 and 15 percent respectively. These data demonstrate in a population of patients with ischemic heart disease, that Q6H dosing with a sustained release procainamide hydrochloride preparation (PROCAN-SR, Parke-Davis) is associated with only a small acceptable variation between maximal and minimal serum procainamide and N-acetylprocainamide concentrations. This preparation should, therefore, offer greater patient convenience and compliance without sacrificing antiarrhythmic efficacy.
Records from 18 subjects with angiographic idiopathic mitral valve prolapse, 28 subjects with merely exaggerated posterior mitral leaflet systolic bulging, and 100 subjects with normal hemodynamic and angiographic findings were compared with regard to age, sex, height, weight, ponderal index (height/3 square root weight), auscultatory and echocardiographic abnormalities. Chest x-ray films available for subjects with mitral valve prolapse were reviewed. The ponderal index of subjects with mitral valve prolapse (13.1 +/- 0.8) differed from that of subjects with merely exaggerated posterior mitral leaflet systolic bulging (12.6 +/- 0.7) (P less than 0.02) and from that of subjects without angiographic abnormality (12.3 +/- 0.8) (P less than 0.001). The three groups differed in ponderal index when equated statistically for age, height, weight, and sex (P less than 0.001). Among mitral valve prolapse patients, an asthenic habitus occurred independent of the presence of thoracic skeletal abnormalities.
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The first adult patient with catheterization-proven isolated rheumatic heart disease who demonstrated the electrophysiologic findings of "persistent atrial quiescence" is described. Metabolic causes of transient atrial sequence were effectively excluded by clinical history and appropriate laboratory studies. Atrial quiescence may be the electrophysiologic expression of end-stage rheumatic atrial pathology seen only in cases of advanced, surgically uncorrected rheumatic mitral valve disease.
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Two dimensional echocardiographic criteria for bicuspid aortic valve recognition have greater specificity than previously proposed M-mode echocardiographic criteria. The potential clinical use of the two dimensional technique is, however, limited by the technical inability to image adequately the aortic valve leaflets in many patients. One hundred consecutive adult patients undergoing two dimensional echocardiography were prospectively studied. Valve cusp number could not be determined because of dense calcification in eight patients. A bicuspid aortic valve was diagnosed in a single subject. A parasternal short axis view disclosed three commissures (diastolic "Y" configuration) in only 26 patients. Technically adequate parasternal short axis imaging was more likely in younger patients and in non-smokers. In patients not successfully imaged from the parasternal approach, an anteriorly tilted apical four chamber view showed a diastolic "Y" configuration in an additional eight cases. Considering the high prevalence in our population of incomplete two dimensional echocardiographic aortic valve leaflet imaging, angiographic and/or pathological studies must be performed to establish the correlation between these incomplete echocardiographic patterns and aortic valve anatomy if two dimensional echocardiography is to have widespread application in the diagnosis of the congenital bicuspid aortic valve.