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Biomedical subjects

R E Goldstein

Publications and source records attributed to R E Goldstein.

At least 163 records · Page 9Linked to original sources
PubMed1977

Sudden infant death syndrome (SIDS). Echocardiographic studies in relatives of infants with SIDS.

Echocardiographic studies were performed in 42 sets of parents who had at least one infant with Sudden Infant Death Syndrome (SIDS). Asymmetric septal hypertrophy (ASH) was detected by echocardiography in one member of only 5 percent of the 42 sets of parents. Echocardiograms were also obtained in three other sets of parents who had infants with SIDS (selected because their infants showed small foci of disorganized cardiac muscle cells in the ventricular septum, similar to those present in patients with typical ASH but less marked in severity). ASH was present in one member of each of these three sets of parents. Ventricular septal-to-posterobasal left ventricular wall thickness ratios in the five subjects in this study with echocardiographically determined ASH ranged from 1.3 to 1.7, although only one individual showed marked thickening of the ventricular septum (22 mm). Thus, SIDS and ASH do not appear to be commonly associated conditions.

Cardiomyopathy, Hypertrophic↗
PubMed1977

A new method for quantifying ventricular regularization during atrial fibrillation.

Atrial fibrillation (AF) characteristically results in random variation of the intervals between successive ventricular depolarizations. However, when a patient with AF is treated with excessive amounts of digitalis, regular junctional rhythms may occur. The detection of "regularization" of the ventricular rhythm in patients with AF may signal early digitalis toxicity. In this paper, we describe a new method for quantifying the extent of ventricular regularization by the statistical analysis of the intervals between successive ventricular depolarizations (R-R intervals). This method yields a single index (Z score) which reflects the degree to which a sequence of R-R intervals deviates from a random distribution. Simulation studies demonstrate that our method is sensitive to "regularization" of as little as two to four percent of R-R intervals, even when equal intervals occur in small groups that might easily escape detection by visual electrocardiographic interpretation. Analysis of records from six nondigitalized subjects in AF shows that the sequence of R-R intervals is usually random, or very nearly so. Records obtained from the same patients when digitalized often demonstrate more regularized activity, reflected by an index (Z score) which is higher than expected from chance deviation if a random process is assumed. Preliminary data also suggeest that exercise is associated with substantial regularization of ventricular depolarization.

Atrial Fibrillation↗
PubMed1976

Beneficial effect of lidocaine on ventricular electrical stability and spontaneous ventricular fibrillation during experimental myocardial infarction.

Several studies have questioned the efficacy of lidocaine in reducing the incidence of ventricular fibrillation shortly after acute myocardial infarction when arrhythmogenic mechanisms may be different from those operative several hours later. To determine whether lidocaine inhibits the occurrence of early ventricular fibrillation, the left anterior descending and septal coronary arteries were occluded at their origins in open chest anesthetized dogs. Fourteen of 16 control dogs died with ventricular fibrillation. Fifteen dogs received two different dose regimens of lidocaine before coronary occlusion. Of the 11 treated dogs maintaining lidocaine bl), 6 survived (P less than 0.05). Five dogs received the larger dose; all died, four having blood levels of 6.3 mug/ml or greater at the time of death. Ventricular fibrillation threshold also increased in six of eight dogs when lidocaine was administered after coronary occlusion. It is concluded that lidocaine at blood levels of 1.2 to 5.5 mug/ml significantly reduces the incidence of ventricular fibrillation early after coronary occlusion. Administration of this agent therefore may be of particular value in the early phase of acute myocardial infarction.

Animals↗
PubMed1976

Potential role of QT interval prolongation in sudden infant death syndrome.

To investigate the possibility that a genetically transmitted cardiac abnormality is involved in the genesis of the sudden infant death syndrome (SIDS), 42 sets of parents who had at least one infant with SIDS were studied by electrocardiography. Prolongation of the QT interval was present in at least one member of 11 (26%) sets of parents. In families in which QT interval prolongation was found in a parent, prolonged QT interval was also present in 39% of the siblings of infants with SIDS, suggesting an autosomal dominant pattern of inheritance. In addition, an infant with "near-miss" SIDS showed marked prolongation of the QT interval. Thus, our data suggest that prolonged QT interval may play a role in a considerable proportion of sudden and unexpected infant deaths. However, definitive confirmation of the relation between QT interval prolongation and SIDS will require large prospective investigations.

Adolescent↗
PubMed1976

Protection of ischemic myocardium by nitroglycerin: experimental and clinical results.

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.

Animals↗
PubMed1975

Coronary collateral function in patients without occlusive coronary artery disease.

Little is known of the functional capacity of coronary collaterals in humans without occlusive coronary artery disease. We, therefore, measured peripheral coronary pressure (PCP) and retrograde flow (RF) from coronary arteries at aortic valve replacement in seven patients without occlusive coronary artery disease. Using a T-connection interposed in left (LCA) and right (RCA) coronary perfusion lines, data were obtained during brief proximal occlusion of each line. PCP was expressed as a fraction of perfusion pressure (PP), and collateral resistance (CR) was calculated as PP/RF. Median values were as follows: (a table was included). In contrast, previous studies of well-collateralized distal segments of diseased coronary arteries revealed mean RF 15.7, CR 5.1 and PCP/PP 0.50. Under the conditions of study, all vessels interconnecting the non-diseased RCA and LCA delivered flow and pressure less readily than collaterals to a single distal segment of a diseased coronary artery. Thus, collaterals in patients without diseased coronary arteries have an extremely limited capacity to transmit either flow or pressure. The absolute values of RF were small relative to the muscle mass perfused by each coronary artery, suggesting that perfusion of only one coronary artery in man during operation may not provide substantial perfusion for large portions of myocardium. Comparison of performance of collaterals supplying atherosclerotic and nonatherosclerotic coronary arteries indicates that proximal occlusion may be an important factor stimulating enhancement of collateral function. Moreover, the nitroglycerin-induced improvement in collateral function seen in patients with chronic occlusive coronary disease was not demonstrable in patients without coronary occlusion. Thus, coronary collaterals may acquire nitroglycerin responsiveness as a result of changes induced by chronic coronary occlusion.

Adult↗
PubMed1975

Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease.

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.

Animals↗
PubMed1975

Impairment of autonomically mediated heart rate control in patients with cardiac dysfunction.

Patients with cardiac disorders have defective parasympathetic control of heart rate. To evaluate the possibility of similar changes in sympathetic control of heart rate, we compared reflex chronotropic responses to 80 degree upright tilt and nitroglycerin-induced hypotension in 31 cardiac patients and 7 normal individuals before and after partial parasympathetic blockade with atropine. Tilting revealed an attenuation of the normal heart rate increase in patients; the magnitude of this defect was greatest in patients with more severe symptoms (class III) and evidence of left ventricular dysfunction (the heart rate increase averaged 25 plus or minus 3 beats/min in normal subjects, 12 plus or minus 2 beats/min in class I-II patients, and 7 plus or minus 1 beats/min in class III patients). Class III symptoms due to mechanical causes (mitral stenosis), however, were not associated with this defect. A marked reduction in heart rate rise with hypotension was seen only in those class III patients without mitral stenosis (0.4 plus or minus 0.1 beats min-minus 1 mm Hg-minus 1 vs. 3.0 plus or minus 0.5 beats min-minus 1 mm Hg-minus 1 in normal subjects). This abnormality also persisted after atropine administration, thus confirming a defect in the sympathetic as well as the parasympathetic component of baroreceptor-mediated reflex heart rate control in patients with cardiac dysfunction. Infusions of isoproterenol produced equivalent rises in heart rate in patients and normal individuals, excluding a reduction in beta-receptor responsiveness as a cause of impaired sympathetic influence. Norepinephrine depletion, however, is a well-recognized concomitant of cardiac failure. It is possible that the reduction in sympathetically mediated heart rate responses results in part from depletion of the sympathetic neurotransmitter.

Adolescent↗