Differentiation between ischemic and nonviable myocardium.
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Blood Pressure↗
Biomedical subjects
R H Helfant
Publications and source records attributed to R H Helfant.
Intervention ventriculography. Comparative value of nitroglycerin, post-extrasystolic potentiation and nitroglycerin plus post-extrasystolic potentiation.
The comparative value of nitroglycerin (TNG), post-extrasystolic potentiation (PESP) and their combination (TNG + PESP) to unmask asynergic residual contraction was examined, each patient serving as his own control. Twelve of 13 hypokinetic zones improved both with TNG and PESP. One remained unchanged with either. Of 15 akinetic zones, four improved with both TNG and PESP, while ten remained unchanged. One akinetic zone, although improved with TNG, remained unchanged with PESP. Four dyskinetic zones did not change with either. Six asynergic zones responding to TNG alone demonstrated further augmentation with TNG + PESP. However, none of 13 TNG unresponsive zones improved with TNG + PESP. Thus, TNG, PESP, and TNG + PESP are each equally capable of unmasking asynergic residual contractile ability.
Cardiac Output↗
Reversible asynergy. Histopathologic and electrographic correlations in patients with coronary artery disease.
Histopathologic-electrographic studies of ventriculography depicted nitroglycerin responsive and unresponsive asynergic areas were performed in 25 patients. Of 29 areas, 12 improved with nitroglycerin, showing less than 10% muscle loss. Seventeen unimproved zones demonstrated significant fibrosis. Epicardial electrograms showed R waves in eight of nine improved zones. Of 11 unimproved zones, eight had Q waves. Histopathologic-electrographic data from five responders showed less than 10% muscle loss, of whom four had epicardial R waves. Six unresponsive areas had significant fibrosis, with a QS over four. Thus, nitroglycerin responsive asynergic areas are generally comprised of histologically intact myocardium and are associated with epicardial R waves.
Adult↗
Correlation of pathologic Q waves on the standard electrocardiogram and the epicardial electrogram of the human heart.
To evaluate the relationship between abnormal Q waves on the standard ECG and localized ventricular excitation, unipolar epicardial electrograms were recorded over the left ventricle during aortocoronary bypass surgery in 36 patients. Of 20 without standard ECG Q waves, six had abnormal epicardial Q waves, three anterioly and three inferiorly. Of 16 patients with standard ECG Q waves, four had both precordial and anterior epicardial Q waves while seven had Q waves in leads III and aVF and inferior epicardial Q waves. Three of the 14 had Q waves in both precordial and inferior leads of the ECG but epicardial Q waves only from the antero-apical region in two and only from the inferior wall in one. Two patients with Q waves in both III and aVF had no epicardial Q waves. Thus, the standard electocardiogram underestimates epicardial Q waves. If Q waves are present in the standard ECG, they correlate with the presence, although not invariably the location of Q waves on the epicardial electrogram.
Cardiac Catheterization↗
Reversible asynergy and its determinants.
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Angiocardiography↗
Penetrating injury of the chest and coronary arteriovenous fistula.
An unusual case of coronary artery fistula, due to a stab wound in the chest in a 17-year-old male patient, with a resultant acute inferior myocardial infarction is presented. At surgery, complete transection of the right coronary artery was found, which formed a fistulous communication with both the right atrium and the right ventricle. The development of a continuous murmur in the period immediately after the injury, the absence of hemopericardium, and multiple cardiac-chamber involvements were unique features of the case. The inferior myocardial wall was akinetic due to infarction and did not improve following revascularization surgery. A brief review of the literature is also presented.
Adolescent↗
Nitroglycerin and ventricular performance. Differential effect in the presence of reversible and irreversible asynergy.
The effect of nitroglycerin administration on left venticular performance relative to its ability to improve contraction of asynergic zones was examined in 66 patients with coronary artery disease, divided into those whose asynergic zones responded following nitroglycerin administration and those in whom no response was observed. In the responsive group with asynergy of more than one segment, the ejection fraction improved (P less than 0.001), while in the unresponsive group, it decreased (P less than 0.05). Similarly, in patients with one-segment asynergy, the responsive group exhibited a significant increase in ejection fraction P less than 0.001), while the unresponsive group showed no change. The stroke volume index remained unchanged in the responsive group with asynergy of more than one segment, while it decreased significantly (P less than 0.05) in the unresponsive patients. Left ventricular pressures and volumes changed to a similar degree after nitroglycerin administration in all of the patients, regardless of the responsiveness of asynergic zones. It is concluded that nitroglycerin administration results in a differential effect on total left ventricular performance depending on the responsiveness of asynergic zones.
Blood Pressure↗
Nitroglycerin in experimental myocardial infarction. Effects on regional left ventricular length and tension.
Controversy has existed concerning the value of nitroglycerin therapy in acute myocardial infarction. With use of Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges, the effects of nitroglycerin (30 mug/kg intravenously) were studied on local tension and length characteristics of the ischemic, border and nonischemic zones of the left ventricle in 10 open chest dogs. In the nonischemic zone total tension increased to 144.8 +/- 13.6 (mean +/- standard error of the mean) percent (P less than 0.005) of control levels, and segment length decreased to 79.4 +/- 4.4 percent (P less than 0.01) with infusion of nitroglycerin 15 to 30 minutes after coronary ligation. Changes were similar in the groups given nitroglycerin 45 to 60 minutes and 2 to 3 hours after ligation. The border zone exhibited an increase in total tension to 132.3 +/- 8.4 percent (P less than 0.005) of control level and a decrease in segment length to 79.0 +/- 2.4 percent (P less than 0.001) in the 15 to 30 minute group. In the 45 to 60 minute group, tension increased to 117.9 +/- 4.8 percent (P less than 0.005), whereas length decreased to 86.8 +/- 1.4 percent (P less than 0.001); and in the 2 to 3 hour group tension increased to 124.9 +/- 6.0 percent (P less than 0.005), and length decreased to 91.9 +/- 3.5 percent (P less than 0.001). The decrease in magnitude of responsiveness in the 45 to 60 minute and 2 to 3 hour postligation groups compared with the 15 to 30 minute postligation group was highly significant (P less than 0.005). The central ischemic zone showed no significant change in tension or length in any group. Maximal response to nitroglycerin administration in both tension and length parameters was observed within 30 to 60 seconds and was concomitant with a decrease in systolic pressure to 73.3 +/- 1.9 percent (P less than 0.001) and an increase in heart rate to 107.2 +/- 1.0 percent. Nitroglycerin improves the contractile performance of the nonischemic and border zones after coronary occlusion without affecting the central ischemic zone. However, the border zone exhibits a progressive decrease in contractile response as a function of time. These data suggest that nitroglycerin has the overall effect of functionally reducing the extent of the ischemic area and strongly supports its potential clinical usefulness in acute myocardial infarction.
Animals↗
Q waves and ventricular asynergy: predictive value and hemodynamic significance of anatomic localization.
Two hundred sixteen consecutive patients were evaluated to determine the value of pathologic Q waves in predicting the presence and severity of ventricular asynergy. Of 64 patients with pathologic Q waves, 95 percent demonstrated asynergy. Q waves in the anterior leads denoted asynergy in 30 of 30 patients, anterior asynergy in 29 of 30 and an anterior aneurysm in 25. Q waves in the inferior leads indicated asynergy in 30 of 33 patients, inferior asynergy in 25 of 30 and an associated aneurysm in 19. Conversely, of 52 patients with an aneurysm, 44 also had pathologic Q waves. If Q waves were present, 72 percent of asynergic zones exhibited akinesis or dyskinesis; however, in the absence of Q waves an aneurysm was present in only 22 percent (P less than 0.0001). Hemodynamically, anterior asynergy, whether defined by Q waves or by ventriculography, was associated with more left ventricular dysfunction than was inferior asynergy (P less than 0.01). Of 21 patients with a cardiomyopathy, none had pathologic Q waves. The data indicate that pathologic Q waves can aid significantly in predicting the presence and location of a severely asynergic zone. Although their absence does not exclude the possibility of asynergy, the latter is much less likely and, if present, amy be of milder form.
Cardiac Catheterization↗
Digitalis in experimental acute myocardial infarction. Differential effects on contractile performance of ischemic, border and nonischemic ventricular zones in the dog.
The effects of digoxin priming dose of 0.04 mg/kg body weight followed by infusion of 0.02 mg/kg per min) on local tension and length characteristics of the nonischemic, border and ischemic left ventricular zones were studied in 30 dogs using Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges. Total tension in the nonischemic zone increased to 130.9 plus or minus 5.3 percent (P smaller than 0.001) of the control level in association with parallel changes in preejection and ejection tension and rate of rise of tension when infusion of digoxin was instituted 15 to 30 minutes after ligation. Consistent increases in tension variables were noticed when infusion of digitalis was initiated 45 to 60 minutes or 2 to 3 hours after ligation. Segment length remained unchanged. In the border zone, total tension decreased to 68.9 plus or minus 5.9 percent (P smaller than 0.01) after infusion of digitalis. When infusion of digitalis was instituted 45 to 60 minutes or 2 to 3 hours after occlusion, similar increases in total tension and other tension variables were seen. Segment length again showed no significant changes. There was an increase in total tension in 5 of the 12 ischemic zones studied when digitalis was infused 15 to 30 minutes after coronary arterial ligation, whereas a consistent (3 to 5 percent) decrease in tension was observed when infusion of digitalis was instituted 45 to 60 minutes and 2 to 3 hours after coronary occlusion. There was no increase in segment length. In summary, digitalis uniformly increased contraction of the nonischemic and border zones after coronary arterial ligation, but the effects on contraction and aneurysmal bulging in the ischemic zone were minimal.
Animals↗
Contractile and electrophysiological responses to progressive digitalis toxicity.
Contractile force and intraventricular conduction during progressive ouabain infusion were examined in 15 dogs using a Walton-Brodie strain gauge arch and sequential atrial and bundle of His pacing. This permitted: (1) contractile force determination; (2) overdrive of arrhythmias; (3) maintenance of normal contraction sequences; (4) 'normal' ventricular depolarization; (5) rate control; (6) conduction measurements of the H-V interval (His-Purkinje conduction), QRS (intramyocardial conduction), and H-S interval (total intraventricular conduction). Contractile force increased 21.2 plus or minus 4.3% at the onset of toxicity. After toxicity, there was a significant further increase (P smaller than 0.01) to 50.1 plus or minus 12.4%. However, immediately before ventricular fibrillation, a 43.8 plus or minus 8.2% decrease occurred (P smaller than 0.01). H-V time showed no change (from 30 plus or minus 2.7 to 31.5 plus or minus 2.4 ms) at the onset of toxicity but after toxicity, it lengthened to 40.5 plus or minus 3.1 ms (P smaller than 0.05). QRS did show significant prolongation (69.5% plus or minus 5.3 to 79.5 plus or minus 6.9 ms; P smaller than 0.05) at the onset of toxicity, but this was more marked (79.5 plus or minus 6.9 to 130.5 plus or minus 8.1 ms; Pplus or minus 0.01) after toxicity. H-S time was significantly prolonged (99.5 plus or minus 6.2 to 111.0 plus or minus 8.9 ms) before (P smaller than 0.02) and after (P smaller than 0.01) toxicity (111.0 plus or minus 8.9 to 171.1 plus or minus 10.6 ms). During toxicity there is progressive increase in contractile force with continued ouabain infusion Progressive prolongation of intramyocardial conduction occurs in nontoxic and toxic doses, but His-Purkinje conduction is prolonged only in supratoxic doses.
Animals↗
Corrected sinus node recovery time. Experimental physiologic and pathologic determinants.
To determine the factors affecting reproducibility of sinus node recovery time, the effects of basic pacing rate, pacing duration, milliamperage, vagal and beta-adrenergic stimulation, and sinud node injury, as well as its instantaneous and daily reproducibility, were studied in 36 anesthetized dogs. Corrected sinus node recovery time (CSNRT) showed a mean variation of 9.8 plus or minus 0.4 msec at an atrial pacing rate of 200 beats/min and 29.8 plus or minus 8 msec at an atrial pacing rate of 140 beats/min (P smaller than 0.05). CSNRT increased progressively from 55.4 plus or minus 10 msec to 103.7 plus or minus 13 msec with increase in pacing rate from 140 beats/min to 200 beats/min. It was reproducible when atrial pacing was carried out for 1-5 min, although a wide variation (10-30 msec) was seen from 7-60 minutes (P smaller than 0.05). This measurement was reproducible on two consecutive days and was unaffected by changes in milliamperage. Vagal stimulation consistently prolonged the CSNRT while beta-adrenergic stimulation decreased it from 132.9 plus or minus 34.5 msec to 50.0 plus or minus 6.5 msec. Sinus node injury consistently prolonged CSNRT at all paced rates. In summary, CSNRT is reproducible only if the same pacing rate and duration are utilized. Since vagal stimulation and sinus node injury prolong this measurement while beta-adrenergic stimulation shortens it, an "abnormal" CSNRT should be assessed in terms of the possible influence of the autonomic nervous system as well as sinus node dysfunction per se.
Animals↗
Electrophysiologic effects of coronary occlusion and reperfusion. Observations of dispersion of refractoriness and ventricular automaticity.
UNLABELLED: In order to determine the electrophysiological changes that occur during coronary occlusion and following reperfusion, 19 mongrel dogs were studied. Refractory periods were determined by the extrastimulus method in nonischemic and ischemic zones prior to and after variable periods of left anterior descending artery occlusion and reperfusion. After 15-30 minutes of occlusion, refractory periods in the nonischemic zones remained unchanged while in the ischemic zone they shortened by 17%, resulting in a dispersion of refractoriness. Within three minutes of reperfusion, arrhythmias appeared together with a marked directional change of refractory periods to a prolongation by 34% (P less than 0.001) in the ischemic zone and by 3% (P less than 0.02) in the nonischemic zone. Refractory periods returned to baseline values after 60 minutes of reperfusion. After 60-90 minutes of occlusion, refractory periods in the nonischemic zones were unchanged whereas in the ischemic zone they demonstrated a decrease by 28% (P less than 0.01), again resulting in a dispersion of refractoriness. Within five minutes of reperfusion, refractory periods in the ischemic zone prolonged by 44% (P less than 0.001). Similar but smaller directional changes were also seen in nonischemic zones. Concomitant with the observed prolongation in refractory periods frequent ventricular ectopic activity was again documented. In addition, refractory periods did not return to control values after periods of observation up to 120 minutes in this group. In seven dogs, complete heart block was induced to ascertain the rate of idioventricular pacemaker and the effect of ventricular overdrive on the escape interval. Control ventricular rates (53.3 +/- 5.7 beats/min) remained unchanged (52.3 +/- 5.6) following coronary occlusion, but decreased to 48.0 +/- 4.4 (P less than 0.05) during reperfusion. Mean control escape intervals (1.8 +/- 0.2 sec) did not change after occlusion (1.7 +/- 0.2 sec) but prolonged to 2.1 +/- 0.2 sec (P less than 0.05) following reperfusion. IN CONCLUSION: 1) sudden prolongation in refractory periods following reperfusion leads to an overshoot resulting in a dispersion of refractoriness temporally related to the onset of ventricular arrhythmias and 2) re-entry, and not enhanced automaticity, appears to be the mechanism for postperfusion arrhythmias.
Animals↗
Determinants of reversible asynergy. The native coronary circulation.
To evaluate the influence of the native coronary circulation on the reversibility of asynergy, ventriculograms before and after sublingual nitroglycerin were performed in 51 patients with coronary artery disease and asynergy. The severity of stenotic lesions and caliber of the distal coronary vessels were determined by comparison with external catheter tip diameter corrected for magnification. Of 42 asynergic zones associated with larger than or equal to 90% proximal coronary occlusion, 27 (64%) were akinetic or dyskinetic while only 11 of 38 zones (29%) with less than 90% occlusion showed akinesis (P less than 0.005). Twenty-six of the 38 asynergic zones (69%) with less than 90% occlusion were reversible in contrast to 19 of the 42 zones (45%) with larger than or equal to 90% occlusion (P less than 0.05). Coronary collaterals were observed in 23 of 42 (55%) zones with larger than or equal to 90% occlusion in contrast to only 11 of 38 zones (29%) with less than 90% occlusion (P less than 0.05). Of the zones with both greater than or equal to 90% occlusion and collaterals, 74% were reversible, in contrast to only 11% without collaterals (P less than 0.001). Of the asynergic zones without collaterals, 63% with less than 90% occlusion were reversible in contrast to only 11% with larger than or equal to 90% occlusion (P less than 0.001). Pathologic Q waves were associated with 24 of 42 zones (57%) with larger than or equal to 90% occlusion compared to only nine of the 38 zones (24%) with less than 90% occlusion (P less than 0.01). The presence of Q waves was associated with a significant decrease in the incidence of reversibility regardless of the degree of coronary occlusion. Excluding the asynergic zones with either collaterals or Q waves, 79% with less than 90% occlusion were reversible in contrast to only 37% with larger than or equal to 90% coronary occlusion (P less than 0.05). In contrast, the caliber of the distal vessel could not be correlated with either the severity of asynergy or the presence of collaterals and was similar in both reversible and irreversible asynergic zones. In summary, larger than or equal to 90% proximal stenosis is associated with severe asynergy which is less likely to be reversible compared to asynergy associated with less than 90% coronary occlusion. In the presence of larger than or equal to 90% occlusion, coronary collaterals are associated with a significantly higher incidence of reversible asynergy and thus appear to serve a protective function. However, the caliber of the distal vessel per se does not effect the severity or reversibility of asynergy.
Cardiac Output↗
Electrophysiologic effects of nitroglycerin during experimental coronary occlusion.
Previous studies have shown that nitroglycerin (TNG) exerts beneficial electrophysiological effects in the setting of acute myocardial ischemia. To investigate the basis for these actions, the effects of TNG during coronary occlusion were studied in 19 anesthetized mongrel dogs. Refractory periods (obtained by extrastimulus method) and conduction times measured from local electrograms were determined in potentially ischemic and nonischemic areas prior to and after varying periods of occlusion of the left anterior descending coronary artery and following administration of TNG (300-400 mug intravenous bolus followed by an infusion titrated to reduce systolic blood pressure by 20 mm Hg). Following 15 minutes of occlusion, refractory periods in the ischemic zones shortened to 83% of control (P less than 0.001) resulting in a difference between refractory periods in the nonischemic and ischemic zones of 17.7%. After TNG administration this difference was decreased to 10.0% (P less than 0.001). However, with periods of occlusion of 60-90 min TNG did not significantly affect the difference of refractory periods. TNG had no significant effects on conduction times in nonischemic or ischemic areas. In six dogs, the effects of coronary occlusion and TNG on ventricular automaticity were examined by induction of complete heart block. The idioventricular rate and ventricular escape intervals after cessation of ventricular overdrive were used as indices of automaticity. Control idioventricular rates (62.5 +/- 3.7 beats/min) remained unchanged following both coronary occlusion (62.0 +/- 3.9) and TNG administration (60.7 +/- 3.2). Similarly, mean control escape intervals (1.84 +/- 0.2 sec) did not change after occlusion (1.78 +/- 0.3 sec) or TNG administration (1.86 +/- 0.2 sec). In conclusion, these observations suggest that 1) TNG enhances the electrical stability of the acutely ischemic myocardium by decreasing the difference of refractory periods between nonischemic and ischemic areas in the immediate period following occlusion, 2) since TNG has no significant effects on ventricular automaticity, its beneficial effects might be limited in suppression of arrhythmias of re-entrant origin.
Animals↗
Update--evaluation of the chest pain syndrome.
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Angina Pectoris↗
Temporal sequence of dynamic contractile characteristics in ischemic and nonischemic myocardium after acute coronary ligation.
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Animals↗
Limitations of myocardial revascularization in restoration of regional contraction abnormalities produced by coronary occlusion.
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Animals↗