Effects of exercise on signal-averaged electrocardiogram.

Signal averaging can be used to assess changes in myocardial activation under a variety of physiological conditions including stress. This study prospectively evaluated patients who underwent rest and exercise recording of signal-averaged electrocardiograms. The 163 patients were divided into three groups based on thallium results: normal (group I), reperfusion (group II), and fixed defect (group III). Patients in group I showed shortening of the high frequency duration (P = 0.02) and the duration of the low amplitude signal (P = 0.024) after exercise. In these patients the terminal root mean square amplitude (RMSA) also increased significantly (P = 0.005). However, patients who were in either group II or group III showed little change in signal averaging measurements after exercise. The amplitude of the QRS in V5 and the RMSA of the total QRS also increased in all groups following exercise, with a lesser increase in the patients with reperfusion by thallium imaging (group II). There was no change among groups in the incidence of ventricular late potentials with exercise. This suggests that patients with ischemia or infarction may not have the same response to an increase in sympathetic tone with exercise as patients without abnormalities of cardiac perfusion. The clinical implications of these findings may include demonstration that an area of slow conduction exists in these latter two groups of patients.

The contraction of stunned myocardium: isovolumetric bulging and wasted ejection shortening in dog heart.

OBJECTIVE: The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. METHODS: Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. RESULTS: With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increased in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. CONCLUSIONS: The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.

Mannitol stimulates atrial natriuretic peptide release in humans.

The purpose of this study was to determine if mannitol stimulates atrial natriuretic peptide (ANP) release in humans and to examine potential mechanisms for this effect. Twenty patients requiring cardiac catheterization were randomized to receive either mannitol (15-g bolus followed by 15% infusion mixed in 75 mmol/L saline at 100 mL/h for 1 hour) or an equal volume of 75 mmol/L saline, intravenously (IV). All measurements were made at three time points: at baseline, at 10 minutes (after the bolus but before radiocontrast administration), and at 60 minutes (after completion of the study). Baseline plasma ANP (PANP) measurements (mean +/- SE) were similar in both groups (saline, 73 +/- 38 pg/mL; mannitol, 62 +/- 11 pg/mL). PANP increased significantly over time for the set of all patients (analysis of variance [ANOVA], P less than 0.05); however, at 10 minutes PANP increased significantly only in the group receiving mannitol (saline, 76 +/- 43 pg/mL; mannitol, 100 +/- 29 pg/mL) (P less than 0.04). Serum osmolality (SOSM), over time for the set of all patients (ANOVA, P less than 0.04). At 10 minutes there were significant increases only in the group receiving mannitol, and after radiocontrast, there were significant increases in both groups for all parameters. Regression analysis demonstrated a significant correlation between the change in PANP and the change in SOSM (P less than 0.04, r = 0.33). In conclusion, intravascular infusion of mannitol or radiocontrast increased PANP levels. The mechanism may be multifactorial, with a potential role for an increase in SOSM and/or PADH.

Effect of postextrasystolic potentiation on systolic bulging of ischemic myocardium.

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined. By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic -9.1 +/- 2.0% to -5.9 +/- 1.7%, p less than 0.008; ejection 2.2 +/- 0.7% to 4.3 +/- 2.0%, p less than 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion. This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.

The effect of ionic contrast medium on the movement of acutely ischemic and nonischemic canine myocardium.

Regional function assessed by ventriculography may be influenced by the hemodynamic effects of rapidly injecting ionic contrast medium. The importance of this after acute coronary occlusion was examined in eight open-chest, anesthetized dogs. The left anterior descending artery was ligated while sonomicrometric segment lengths in the ischemic (IZ) and nonischemic zones (NZ) were measured. Sodium methylglucamine diatrizoate (Renografin-76, 1 ml/kg) was rapidly injected over 3 seconds. Fifteen minutes later, the left ventricular end-diastolic pressure (LVEDP) was rapidly increased to the level reached during injection. Injecting the contrast increased the LVEDP (7.3 +/- 2.5 to 20.1 +/- 2.9 mm Hg, p less than 0.0001) to the same extent as raising LVEDP (7.6 +/- 2.5 to 10.1 +/- 2.9 mm Hg, p less than 0.0001). Injecting the contrast medium increased IZ total percent systolic shortening (% delta L) (-3.90 +/- 4.43% to -2.68 +/- 4.77%, p less than 0.001) by decreasing isovolumic bulging (-6.68 +/- 4.09% to -5.49 +/- 3.33%, p less than 0.001) with little change in ejection % delta L. NZ total % delta L tended to increase (19.03 +/- 6.53% to 19.94 +/- 6.27%, p = 0.015) because of augmented ejection % delta L (13.12 +/- 2.51% to 13.71 +/- 3.10%, p = 0.017) by the Starling mechanism. Increasing the LVEDP had the same effect on IZ and NZ regional shortening as injecting contrast. Thus regional shortening after acute coronary occlusion is affected by the changes in loading conditions with ionic contrast ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmentation of contraction in remote nonischemic zone during acute ischemia.

We studied how left ventricular loading conditions and the size of the ischemic zone affect regional segmental shortening (% delta L) in ischemic (IZ) and remote nonischemic zones (NZ) after acute coronary occlusion. Distal and proximal portions of the left anterior descending artery (group I, 10 dogs) or the left circumflex artery (group II, 10 dogs) were occluded in two stages. Segment length sonomicrometers were placed in the distal and proximal IZ and in the distal and proximal NZ. % delta L was divided into isovolumic and ejection phases. Left ventricular end-diastolic pressure (LVEDP) was decreased 3 +/- 1 mmHg by blood withdrawal and then increased 6 +/- 2 mmHg by blood transfusion before and after distal and proximal coronary occlusions. LVEDP was brought back to its initial value before distal and proximal coronary occlusions. Regional blood flow and total blood flow deficit were measured with microspheres. Similar results were obtained in group I and II experiments. After coronary occlusion, the IZ showed systolic bulging occurring primarily in isovolumic systole. In the NZ, total and isovolumic % delta L increased from control, whereas ejection % delta L did not change. As LVEDP was raised, IZ isovolumic bulging decreased and ejection % delta L was unchanged, whereas NZ isovolumic % delta L decreased and ejection % delta L increased. Thus IZ bulging and NZ isovolumic % delta L changed in opposite directions when load was varied. The larger IZ after proximal coronary occlusion tended to increase the amount of NZ isovolumic % delta L. In conclusion, at low LVEDP NZ augmentation is predominantly caused by an increase in isovolumic % delta L, whereas if LVEDP is increased it is because of an increase in ejection % delta L. In addition, in open-chest animals augmented contraction in the NZ may be related to the size of the IZ.

Contractile function and reserve during acute ischaemia in the canine lateral border zone.

The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone (FNZT less than 0.1), seven were in the border ischaemic zone (FNZT 0.1-0.5), five were in the border non-ischaemic zone (FNZT 0.5-1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was -2.3(5.9%) and in the ischaemic zone -3.5(3.6)% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of changes in afterload on systolic bulging.

It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 +/- 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (% delta L) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Magnetic resonance imaging to evaluate patency of aortocoronary bypass grafts.

To assess the efficacy of magnetic resonance (MR) imaging in evaluating graft patency after coronary bypass surgery, 20 patients who had prior surgery (average 5.5 years, range 1.5 to 14) and recent cardiac catheterization because of chest pain were studied. No patient had surgical intervention or change in symptoms in the time interval between catheterization and MR imaging. These 20 patients had a total of 47 grafts, defined as proximal anastomoses: 20 to the left anterior descending or diagonal artery (LAD), 13 to the left circumflex artery marginal branches (LCX), and 14 to the right coronary artery or posterior descending artery (RCA). The patients underwent cardiac and respiratory gated MR scans in a 0.5 tesla magnet with an echo time of 22 msec and two repetitions in a 128 X 256 matrix. In-plane resolution was 2.7 mm. Every patient had a scan in the transaxial plane and some underwent scanning in the sagittal and coronal planes as well. A graft was considered patent by MR when a signal-free lumen was visualized in an anatomic position consistent with that of a bypass graft, had a lumen larger than the native vessels, was seen on more than one slice, and was seen at a level higher than that of the native vessels. If a known graft was not seen it was considered occluded. The scans were interpreted by consensus of two physicians aware of the operative but not the cardiac catheterization data.(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of coronary vascular reserve in myocardium distal to a fixed coronary stenosis.

In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)