Cessation Of Pacing Research Articles

Left ventricular remodelling and disparate changes in contractility and relaxation during the development of and recovery from experimental heart failure.

Canine pacing induced heart failure is characterised by impaired left ventricular contractility and relaxation, and clinical recovery after cessation of pacing. It is unclear whether the impairment is responsive to adrenergic stimulation. The aim of this study was to assess left ventricular contractility and relaxation and their response to beta adrenergic stimulation during heart failure and after recovery. Eight dogs were paced (250 beats.min-1) for 3 weeks to severe heart failure and recovered for 4 weeks after cessation of pacing. During these periods, haemodynamic and echocardiographic measurements were made with and without beta adrenergic stimulation. At heart failure, impaired left ventricular contractility was evidenced by reduced dP/dt [1412(SD 156) mm Hg.s-1 from 2437(382) mm Hg.s-1 at control, p < 0.01] and a downward displacement of the velocity of circumferential fibre shortening-end systolic wall stress relation. Impaired left ventricular relaxation was evidenced by raised end diastolic pressure [35(6) mm Hg from 7(4) mm Hg at control, p < 0.01] and prolonged relaxation time constant tau [28(4) ms from 17(6) ms, p < 0.01]. The ability of beta adrenergic stimulation to augment contractility was reduced: there was blunted dP/dt response to dobutamine. The ability of beta adrenergic stimulation to shorten relaxation was maintained: there was a similar degree of shortening of tau by dobutamine. At recovery, dP/dt returned to control and the shortening-stress relation moved upward, suggesting return of contractility. The response of dP/dt to dobutamine was restored. However, tau remained prolonged indicating persistent abnormal relaxation. In pacing induced heart failure, there is a dissociation between the normal ability of beta adrenergic stimulation to augment contractility and shorten relaxation, and a differential capacity for recovery of contractility and relaxation.

Patterns of interruption of atrial flutter induced by rapid atrial pacing.

We evaluated the patterns of interruption of atrial flutter (AFl) induced by rapid atrial pacing in 10 patients using standard electrophysiologic techniques. We observed 3 patterns of interruption of AFl: 1) interruption resulting from block of an orthodromic wavefront within the reentry loop in 5 patients; 2) interruption when pacing impulses no longer captured all of the recording sites in the atrium during rapid atrial pacing in 2 patients, and 3) interruption with 1 echo wave after the cessation of pacing in 3 patients. These findings suggest that there are patterns of interruption of AFl other than that resulting from a simple block of an orthodromic wavefront within the reentry loop.

A single five minute period of rapid atrial pacing fails to limit infarct size in the in situ rabbit heart

Rapid pacing has been shown to precondition the dog heart against ischaemic dysrhythmia. The aim of this study was to determine whether rapid pacing could also limit infarct size. Rabbits (n = 5) were rapidly paced via the left atrium at 420-480 beats.min-1. Five min of rapid pacing and 10 min of recovery in sinus rhythm were followed by 45 min of regional ischaemia and 120 min of reperfusion. Control rabbits (n = 9) were treated identically without prior rapid pacing. Infarct size was determined in both groups using tetrazolium and expressed as a percentage of the area at risk demarcated by fluorescent microspheres. In a separate series of experiments, rapidly paced Langendorff perfused rabbit hearts (n = 9) were used to determine coronary flow under perfusion conditions designed to simulate the in vivo situation during rapid pacing. Rapid pacing caused a fall in systolic pressure from 91.4(SEM 4.5) to 47.0(5.9) mm Hg (p < 0.01) and diastolic pressure from 67.2(2.9) to 23.6(3.2) mm Hg (p < 0.01). Both recovered within 30 s of cessation of pacing. During rapid pacing the action potential duration shortened from 192(13) to 128(5) ms (p = 0.01) and developed electrical alternans (n = 4). Following rapid pacing the ECG showed either ST depression or T wave inversion (n = 4). Despite these profound changes, rapid pacing did not reduce infarct size v control [52.7(4.6)% v 60.8(9.1)% of the area at risk, respectively]. The in vitro experiments estimated that rapid pacing would result in a reduction in coronary flow to 44% of that in sinus rhythm without a significant rise in lactate efflux. In our model, pretreatment with rapid pacing fails to reduce infarct size. The most likely reason for this is that rapid pacing at a rate of 480 beats.min-1 does not cause myocardial ischaemia of sufficient severity to trigger the preconditioning response.

Use of Monophasic Action Potentials to Evaluate Postpacing T Wave Changes

We examined the relationship between postpacing T wave changes and monophasic action potentials recorded from the ventricle in dogs. MAPs were recorded from the right and left ventricle before and after cessation of pacing. The duration of the MAP was calculated as the time in milliseconds from the upstroke to 90% repolarization (MAPD90). T waves in limb leads were flat or had a biphasic pattern, eventually becoming negative after pacing. The Q-T interval of the escape beat after pacing was prolonged compared with the control. After right ventricular pacing, the average duration of MAPD90 in the right ventricle, but not in the left ventricle, was prolonged. (right MAPD: control 275 +/- 10 ms; after pacing: 311 +/- 17 ms, p < 0.05; left MAPD: control: 266 +/- 23 ms, after pacing: 284 +/- 26 ms, NS). After left ventricular pacing, the average duration of MAPD90 in the left ventricle, but not in the right ventricle, was prolonged (right MAPD: control: 247 +/- 75 ms, after pacing: 287 +/- 39 ms, NS; left MAPD: control: 257 +/- 23 ms, after pacing: 303 +/- 25 ms, p < 0.05). Furthermore, the average duration of MAPD90 at the pacing site became progressively prolonged over time. These results suggest that myocardial cells retain the memory of abnormal repolarization associated with pacing.

Altered cardiac hemodynamic and electrical state in normal sinus rhythm after chronic dual-chamber pacing for relief of left ventricular outflow obstruction in hypertrophic cardiomyopathy

Dual-chamber (DDD) pacing relieves left ventricular (LV) outflow tract obstruction in patients with hypertrophic cardiomyopathy. The reduction in LV outflow gradient persists in some patients after cessation of pacing. Twelve-lead and signal-averaged electrocardiograms were obtained before and after 12 weeks of DDD pacing in 18 patients with obstructive hypertrophic cardiomyopathy to determine whether the altered hemodynamic state after chronic pacing is accompanied by electrical changes. Hemodynamic studies were performed at baseline and at follow-up. Signal-averaged electrocardiograms were obtained using a Corazonix Predictor and bidirectional filters at 25 Hz to a noise level of <0.5 μV. At follow-up, LV outflow tract gradients were reduced significantly during DDD pacing and with cessation of pacing in sinus rhythm by 56 ± 10 and 47 ± 10 mm Hg, respectively (p < 0.001). There was no simple relation between changes in LV outflow tract gradient and in the electrocardiogram. For example, amplitude of the R wave in V 5,6 was reduced by ≥0.5 mv in 4 patients, unchanged in 12 and increased in 2. Similarly, the S wave in leads V 1,2 was reduced in 7 patients, unchanged in 7 and increased in 4. The T wave became more negative (≥0.1 mv) in leads II, III, aVF and V 5,6 in 13 patients and more positive in leads I and aVL in 12. The QRS was also altered by signal-averaged electrocardiographic criteria; duration of the total QRS and root-meansquare voltage of the QRS of the filtered Y axis increased (106 ± 12 to 112 ± 13 ms [p = 0.036] and 170 ± 82 to 195 ± 102 μV [p = 0.059], respectively). In conclusion, chronic DDD pacing significantly reduces obstruction to LV outflow, and after discontinuation of chronic DDD pacing, there is evidence of altered mechanical as well as electrical myocardial state.

A possible mechanism for pacemaker-induced T-wave changes.

The genesis and the significance of pacemaker-induced T-wave changes remain unclear. Changes in body surface potential mapping (BSM) were observed and compared with resting thallium-201 myocardial scintigraphy (T1-SC) findings before, during and after ventricular pacing (VP) in 10 patients with various bradyarrhythmias. All studies were performed with the patients taking no medication. In all patients, isoarea QRST maps showed a characteristic abnormal dipolar pattern with positive values distributed over the upper chest and negative values over the lower chest during VP at a physiological rate for 14 days or more. These abnormalities were preserved almost completely after pacing was terminated; and coincided with deep T-wave inversions in leads II, III, aVF and V4-6. In three patients, BSM performed before VP showed normal QRST isoarea maps with positive values distributed over the left lower chest. All patients in whom resting T1-SC was performed during chronic VP showed transient perfusion defects in the posteroinferior (seven cases) or inferolateral (one case) left ventricular wall. In three patients, T1-SC was performed before VP and showed a normal distribution. Both the pacing-induced perfusion defects and the T-wave abnormalities remained unchanged 2 h after ceasing VP, were attenuated 7 days later and disappeared within a month. These findings suggest that chronic ventricular pacing may produce myocardial ischaemia, and that it persists for a certain period after the cessation of pacing, resulting in post-pacing T-wave inversion.

Temporal alterations in peripheral vascular responsiveness during both the development and recovery from pacing-induced heart failure.

The responsiveness of both the in vitro dorsal pedal artery and in vitro saphenous vein to alpha-adrenergic agents and prostaglandin F2 alpha was evaluated at baseline (prior to the onset of rapid ventricular pacing), at 1 week of pacing (mild heart failure), and 4 weeks after pacing when there was recovery from congestive heart failure. Eleven dogs were paced at 250 beats/min for 1 week and 7 dogs were paced for 3 weeks at 250 beats/min and allowed to recover from pacing for a further 4 weeks. At 1 and 4 weeks of recovery, compared to control, the maximal responsiveness of the dorsal pedal artery to norepinephrine was increased from 5.7 +/- 0.9 to 12.9 +/- 3.3 and 18.6 +/- 1.0 g/mm2, respectively. A similar finding was observed in the saphenous vein. The response of the artery to the selective alpha 1-agonist, phenylephrine, was also enhanced at 1 week. Moreover, the response of the artery and vein to phenylephrine was enhanced further at 4 weeks of recovery. In contrast, the response to the selective alpha 2-agonist, BHT 920, remained unaltered at these time points compared to control. Oxymetazoline, an agent used to differentiate between alpha 1-subdivisions, produced a significantly higher maximal response at 4 weeks of recovery (18.4 +/- 1.6 g/mm2 for the artery and 27.7 +/- 2.6 g/mm2 for the vein) compared to control (8.2 +/- 0.5 g/mm2 for the artery and 10.3 +/- 0.8 g/mm2 for the vein). The artery also displayed lower EC50 values for norepinephrine and phenylephrine at 1 week (0.7 and 2.2 microM, respectively) and 4 weeks of recovery (0.9 and 3.1 microM, respectively) compared to control (6.0 and 9.0 microM, respectively). In contrast, the only significant decreases in EC50's in the vein were the norepinephrine and oxymetazoline at 1 week of pacing (0.2 and 0.06 microM, respectively) compared to control (1.5 and 0.09 microM, respectively). The maximal tension developed to PGF2 alpha was enhanced after 1 week of pacing in both vessels and persisted 4 weeks following the cessation of pacing. Compared with control, EC50 values for PGF2 alpha were decreased at 1 and 4 weeks of recovery. We conclude that differences exist in peripheral vascular reactivity to both alpha 1-adrenoceptor agents and PGF2 alpha at 1 week of pacing and 4 weeks of recovery from pacing. Furthermore, the subtle reactivity differences between the artery and vein reflect different populations of alpha 1-adrenoceptors possibly associated with different signal transduction processes.

Distinction between metabolic and myogenic mechanisms of coronary hyperemic response to brief diastolic occlusion.

We monitored an index of coronary vascular resistance (mean aortic pressure/mean coronary flow) in 19 heart-blocked conscious dogs paced at 60 beats/min and instrumented with an aortic pressure catheter, left circumflex artery electromagnetic flow probe, and a coronary occluder. Cessation of pacing for a single beat resulted in a long diastole control (LDC) intervention beat of 2-second duration characterized by a progressive rise in diastolic coronary vascular resistance index. A 400-msec coronary artery occlusion early in a long diastole (LD4) dramatically inhibited the rate of rise in resistance index during the first 600 msec (phase 1) after occlusion. Partial recovery of the resistance index rise rate was evident during the remaining 400 msec (phase 2) of the long diastole. In nine dogs, LDC and LD4 intervention beats were instituted during two conditions of myocardial metabolic activity in which the myogenic stimuli associated with coronary occlusion would be similar: 1) paired pacing and 2) normal pacing plus intravenous adenosine and phenylephrine infusions (AP) to maintain mean aortic pressure and coronary flow at paired pacing levels. During paired pacing, the LD4-LDC differences in phase 1 and 2 resistance index rise rates (-69 +/- 18 and -48 +/- 31 mmHg/ml/sec2, respectively) were greater than during normal pacing plus AP (-32 +/- 14 and -1 +/- 32 mm Hg/ml/sec2, phase 1 and 2, respectively) (p less than 0.05). These differences are consistent with operation of a metabolic mechanism in response to occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversal of Venous Blood Flow with Atrial Tachycardia and Hydrops in Fetal Sheep

The purpose of this project was to characterize the reversal of blood flow in the proximal inferior vena cava (IVC) seen in fetal sheep with pacing-induced atrial tachycardia and hydrops. We successfully operated on seven pregnant ewes at 118-130 d gestation to attach ECG and pacing wires, insert vascular catheters, and place Doppler flow probes around the common aortic trunk and the IVC. We also performed two-dimensional and Doppler ultrasonographic exams at baseline, after initiation of pacing, and daily thereafter. All fetuses developed hydrops. Ultrasonographic appearance of ascites and pleural effusion occurred within 4 h in four fetuses and within 48 h in all fetuses. Atrial pacing did not affect arterial pH or arterial O2 tension, but arterial CO2 tension increased by a small amount. Mean IVC pressure increased 75%, whereas mean aortic pressure remained the same. Concentrations of plasma protein and albumin and the hematocrit did not change with atrial pacing. Doppler ultrasound examination and Doppler IVC flow tracings showed that flow reversal began immediately with atrial pacing and disappeared immediately with cessation of pacing. Reversed flow was 21% of forward flow. Inspection of simultaneous recordings of ECG, Doppler aortic and IVC flows, and aortic and IVC pressure tracings revealed that the reversed blood flow occurred in diastole in conjunction with atrial contraction and, therefore, could not be due to tricuspid insufficiency. Our findings of increased venous pressure and reversed venous blood flow suggest that ventricular function is impaired and further suggest that oxygen supply to the ventricles may not be sufficient for the increased demand.

Syndrome of Diminished Vasodilator Reserve of the Coronary Microcirculation (Microvascular Angina or Syndrome X): Diagnosis by Combined Atrial Pacing and Thallium 201 Imaging—A Case Report

Patients with angina-like chest pain without evidence of epicardial coronary artery disease or coronary arterial vasospasm are becoming increasingly recognized. These are often related to noncardiac causes including esophageal, musculoskeletal, and hyperventilatory or panic states. However, recently a subgroup of such patients are being recognized as having true myocardial ischemia and chest pain on the basis of diminished coronary microvascular vasodilatory reserve (microvascular ischemia or Syndrome X). The authors describe such a patient who was found to have replication of anginal pain associated with a reversible ischemic defect on thallium 201 imaging during atrial pacing, suggesting ischemia in this myocardial segment. Resolution of angina and ST segment electrocardiographic changes of ischemia occurred with cessation of pacing. We believe this is the first report of a patient with this form of myocardial ischemia diagnosed by this method and should be considered in patients with anginal chest pain after significant coronary artery disease and coronary vasospasm have been excluded.

Slow and long-lasting modulation of myocardial repolarization produced by ectopic activation in isolated rabbit hearts. Evidence for cardiac "memory".

Prolonged ventricular pacing induces T wave polarity changes that persist long after cessation of pacing. To examine how ventricular repolarization is modulated by prolonged changes in activation sequence, we studied the effect of ectopic pacing on the distribution of action potential durations (APDs) in nine isolated Langendorff-perfused rabbit hearts. A contact electrode probe was used to map right and left ventricular-epicardial monophasic action potentials during three consecutive changes in stimulus site, that is, 1) during 45 minutes of right atrial pacing, 2) during 120 minutes of right ventricular pacing, and 3) again, during 60 minutes of right atrial pacing. During each of these phases, the effect of activation sequence on repolarization was examined by linear-regression analysis of APD on activation time (AT). Results averaged for all nine hearts showed that during the initial atrial-pacing phase, APD was inversely related to AT (slope [S] = -1.63; r = 0.76), indicating that sites with earlier activation repolarized later. With the onset of ventricular pacing, the inverse correlation between AT and APD disappeared (S = -0.19; r = 0.31). Continuing ventricular pacing, however, produced slow changes in APD that restored the inverse relation (S = -0.71; r = 0.68 at 120 minutes; p less than 0.0002 versus 5 minutes). Switching from ventricular to atrial pacing again perturbed the inverse correlation (S = 0.28; r = 0.35) but at 60 minutes of atrial pacing, a significant inverse correlation was reestablished (S = -1.25; r = 0.53; p less than 0.01 versus 5 minutes). An inverse correlation between AT and APD tends to synchronize repolarization time (RT, the sum of AT and APD).(ABSTRACT TRUNCATED AT 250 WORDS)

Fusion with the Prolonged First Postpacing Interval in Pacing of Ventricular Tachycardia

In cases of recurrent sustained ventricular tachycardia (VT), constant fusion and progressive fusion in the surface electrogram were observed during overdrive pacing of VT. However, following cessation of pacing, the return cycle of VT (stimulus to the first nonpaced QRS) was longer than the VT cycle length. This phenomenon can be explained by orthodromic capture of the exit site of the VT current with a conduction time (stimulus to QRS) exceeding the VT cycle length. This site can therefore be activated during entrainment of VT during the mid-to-terminal portion of the paced QRS complex, resulting in constant fusion.

Influence of hypertension with minimal hypertrophy on diastolic function during demand ischemia.

Hearts with advanced pressure-overload hypertrophy from systemic hypertension have been shown to have an increased susceptibility to the development of diastolic dysfunction in response to tissue hypoxia and ischemia. It is not known if this propensity to develop diastolic dysfunction in response to ischemia is dependent on the presence of a substantial increase in left ventricular mass, or alternatively, is characteristic of hearts subjected to mild chronic hypertension early in the development of cardiac hypertrophy. We tested the hypothesis that systemic hypertension associated with mild left ventricular hypertrophy increases the susceptibility to the development of diastolic dysfunction in response to demand ischemia. The effects of demand ischemia (6 minutes) were studied in hearts from New Zealand white rabbits with chronic systemic hypertension produced by the one-kidney, one-wrap method (n = 15) and compared with age-matched, sham-operated control rabbits (n = 11) with similar left ventricular mass (5.4 +/- 0.2 vs. 5.4 +/- 0.3 g, respectively). The hearts were studied using an isolated, isovolumic (balloon in left ventricle) preparation with absent pericardium that was perfused with fresh whole blood. At baseline, coronary perfusion pressure was 100 mm Hg with comparable coronary flow per gram left ventricular weight; the hearts were paced at a physiological rate of 3 Hz, and the left ventricular balloon volume was adjusted to achieve a left ventricular end-diastolic pressure of 15 mm Hg in both groups. Left ventricular balloon volume was similar in both groups and volume was thereafter held constant. At baseline, left ventricular systolic pressure (114 +/- 4 vs. 95 +/- 3 mm Hg, p less than 0.001) and developed pressure (18.9 +/- 1.2 vs. 15.1 +/- 0.9 mm Hg/g, p less than 0.05) were higher in the hearts from the hypertensive group in comparison with the control group. During the first minute of global ischemia produced by reducing coronary perfusion pressure from 100 to 20 mm Hg, there was an immediate fall in left ventricular systolic pressure in both groups without an increase in diastolic pressure. In response to the superimposition of pacing tachycardia (heart rate, 6 Hz) during the remaining 5 minutes of the period of ischemia, left ventricular developed pressure was comparable. However, isovolumic left ventricular end-diastolic pressure (measured during long diastoles obtained with transient cessation of pacing) rose to a significantly higher level in the hearts from hypertensive rabbits than in those from the control rabbits (29 +/- 3 vs. 18 +/- 2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Alterations in serum sodium in relation to atrial natriuretic factor and other neuroendocrine variables in experimental pacing-induced heart failure

The pathophysiologic role of atrial natriuretic factor and other neuroendocrine variables in relation to serum sodium and renal function was evaluated in 15 conscious dogs with severe chronic ventricular pacing-induced heart failure (250 beats/min for 5.1 ± 0.4 weeks). Six sham-operated dogs observed over an 8 week period served as controls. Development of heart failure was characterized by a progressive increase in plasma norepinephrine, renin activity and aldosterone from control values of 293 ± 15 pg/ml, 1.4 ± 0.4 ng/ml per h and 124 ± 42 pg/ml, respectively, to 1,066 ± 96 pg/ml,10.2 ± 2.4 ng/ml per h and 577 ± 151 pg/ ml (all p < 0.01), respectively, at severe heart failure.In contrast to other neuroendocrine variables, plasma atrial natriuretic factor increased from a control level of 243 ± 74 pg/ml to a peak concentration of 724 ± 149 pg/ml (p < 0.01) at 2 weeks, then declined and plateaued at twice the level of the control value as severe heart failure developed. At severe heart failure, serum sodium decreased from 147 ± 0.6 to 141.8 ± 2.1 mmol/liter (p < 0.05), whereas urea increased from 6.0 ± 0.5 to 7.8 ± 0.6 mmol/ liter (p < 0.05). The change in serum sodium concentration correlated with plasma renin activity and aldosterone (r = −0.77, −0.88, respectively, both p < 0.01), but not with norepinephrine or atrial natriuretic factor. When sinus rhythm was restored, 14 dogs were observed for 48 to 72 h and 8 dogs were followed up for another 4 weeks after cessation of pacing. Recovery from heart failure was characterized by a return of all neuroendocrine variables, serum sodium and urea levels to control values by 48 to 72 h.The unique time profile of atrial natriuretic factor during the developing heart failure suggests that the circulating level of this hormone may not be sufficient to maintain circulatory homeostasis in advanced heart failure. The strong negative correlations among the change in serum sodium and plasma renin and aldosterone support the hypothesis proposed by previous clinical studies that hyponatremia in congestive heart failure is in part mediated by the activation of the renin-angiotensin system.

Systole has little effect on diastolic coronary artery blood flow.

The hypothesis that myocardial systolic contraction attenuates diastolic coronary flow was tested by comparing flow during diastole to flow during a prolonged asystole. The circumflex coronary artery was cannulated and perfused at constant pressure in closed-chest, morphine- and alpha-chloralose-anesthetized dogs. The heart was paced at 80, 120, 160, or 200 beats/min after atrioventricular heart block under control, intracoronary adenosine, and intravenous norepinephrine treatment conditions. Cessation of pacing while holding coronary pressure constant at the previous diastolic pressure resulted in asystolic circumflex flow that initially equaled the previous diastolic flow during heart rates of 80, 120, and 160 in all treatment groups. Initial asystolic circumflex flow was approximately 5% higher than the previous diastolic flow at a heart rate of 200 beats/min, but this was probably due to an artifact. It is concluded that systolic contraction does not limit diastolic coronary flow at heart rates less than 160 beats/min and probably does not at higher heart rates.

Hemodynamic responses to noninvasive external cardiac pacing

Although improvements in noninvasive external cardiac pacing have led to a technique with reliable electrical capture and reduced patient discomfort, hemodynamic responses to this pacing mode have not been described previously. Accordingly, this technique was applied to 16 patients with a clinical diagnosis of angina pectoris undergoing cardiac catheterization. Three patients had normal coronary arteries, whereas the remaining 13 had significant coronary artery disease. All patients had noninvasive pacing at increasing heart rates to 85 percent of age-predicted maximal heart rate. At maximal pacing, all patients demonstrated a rise in atrial, pulmonary artery, and mean aortic pressures. Cardiac index remained unchanged, reflecting parallel increases in arteriovenous oxygen difference and oxygen consumption. One minute after cessation of pacing, pulmonary artery pressure and oxygen consumption remained elevated, whereas arteriovenous oxygen difference returned to baseline with a subsequent rise in cardiac index. Angina occurred in eight patients with coronary artery disease at peak pacing and was accompanied by a rise in left ventricular enddiastolic pressure after pacing. In eight patients without pacing-induced angina, including the three patients with normal coronary arteries, there was no significant change in left ventricular end-diastolic pressure after pacing. It is concluded that noninvasive external cardiac pacing produces a rise in both right and left heart filling pressures and in oxygen consumption that persist after pacing, and may provoke angina and hemodynamic abnormalities consistent with myocardial ischemia. This mode of pacing appears hemodynamically safe with maintenance of cardiac index and aortic pressure at 85 percent of maximal agepredicted heart rate.

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for >24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for ⩾ 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial Rutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two.Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.

Acute decrease in left ventricular diastolic chamber distensibility during simulated angina in isolated hearts.

It is not clear what factors contribute to the prompt and reversible decrease in left ventricular diastolic chamber distensibility during angina pectoris that is induced by an increase in myocardial energy demand due to exercise or pacing tachycardia. To simulate the demand ischemia that occurs clinically during pacing-induced angina, we used isolated, blood-perfused rabbit hearts with restricted coronary flow and increased myocardial energy demand. A constant left ventricular balloon volume model was used to measure left ventricular diastolic chamber distensibility during 6 minutes of low-flow global ischemia, induced by a reduction in coronary perfusion pressure from 100 to 20 mm Hg. To investigate the influence of different levels of myocardial energy demand, the effects of two different heart rates were studied during low-flow global ischemia; pacing tachycardia (6.4 +/- 0.2 Hz, n = 7) was compared with the rabbit's baseline heart rate of 4 Hz (n = 7). Low-flow ischemia caused a marked decrease in contractile function relative to the baseline preischemic state. In the pacing-tachycardia group, myocardial energy demand, as estimated by the rate X systolic pressure product, was significantly greater than in the constant heart-rate group. When tachycardia was imposed during low-flow global ischemia, there was a transient and reversible increase in isovolumic left ventricular end-diastolic pressure from 14 +/- 1 to 25 +/- 4 mm Hg (measured during long diastoles obtained with transient cessation of pacing) in the pacing-tachycardia group, but there was no increase in left ventricular end-diastolic pressure during low flow ischemia in the constant heart-rate group with lower energy demand (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Traumatic internal jugular vein cannulation

A 63-year-old man with acute myocardial infarction complicated by atrioventricular block underwent an insertion of a temporary electrode for cardiac pacing. The posterior approach for right internal jugular vein cannulation was used. A 15-gauge needle was inserted under the sternocleidomastoid muscle aiming at the suprasternal notch with a 30-degree posterior angle of entry. An hour later the patient started to hiccup. The hiccups were resistant to drug therapy and to cessation of pacing. A chest radiograph revealed elevation of the right diaphragm and hematoma on the right side of the trachea, possibly compressing the right phrenic nerve on its route beneath the sternocleidomastoid muscle and the internal jugular vein. Within seven days the hiccups gradually ceased. Our case shows the advantages and complications of internal jugular vein cannulation.

Effect of Intracoronary Diltiazem on ST-Segment Elevation and Myocardial Blood Flow During Pacing-Induced Ischemia

This study was performed to determine if diltiazem can reduce the severity of pacing-induced ischemia independently of its peripheral hemodynamic effects and of increases in ischemic region blood flow. Twelve anesthetized dogs were subjected to atrial pacing and had their left anterior descending coronary arteries (LAD) occluded gradually until ischemia ensued (greater than 10 mV epicardial ST-segment elevation). Cessation of pacing resulted in abolition of ST-segment elevation. ST-segment elevation, as well as peripheral and coronary hemodynamics, was measured during 5-min periods of pacing + LAD stenosis before and 0, 30, and 60 min after treatment with intracoronary (just distal to the stenosis) saline or 1.8 micrograms/kg diltiazem. Myocardial blood flow was measured using radioactive microspheres during pacing, pacing + stenosis, and pacing + stenosis + drug treatment at 60 min. Diltiazem significantly reduced ST-segment elevation approximately 50% at 0, 30, and 60 min compared with elevations seen in animals treated with saline as well as predrug values. No changes in blood pressure, heart rate, or LAD flow occurred with diltiazem. Overall ischemic tissue flow and its transmural distribution were not different with diltiazem compared with saline treatment. Thus, diltiazem can decrease the severity of pacing-induced ischemia independently of its peripheral effects and of increased ischemic region blood flow.