Diagonal Coronary Artery Research Articles

Reduction of Myocardial Necrosis by Positioning the Intra-Aortic Balloon Pump in the Ascending Aorta

The presence of severe peripheral vascular disease may necessitate inserting an intra-aortic balloon pump (IABP) directly Into the ascending aorta. As positioning an 1ABP into the descending aorta may be hazardous and difficult through the ascending aorta, this experimental study sought to determine the effects of positioning an IABP in the ascending aorta on myocardial recovery during urgent surgical revascularization. The second and third diagonal coronary arteries in 30 pigs were occluded with snares for 90 min followed by 30 min of cardioplegic arrest and 180 min of reperfusion with the snares released. During the period of coronary occlusion, ten pigs received an IABP in the descending aorta, ten had an ascending aorta IABP and ten received no IABP support. The best recovery of wall motion, least tissue acidosis and lowest area of necrosis occurred when an IABP was positioned in the ascending aorta. It is concluded that myocardial recovery is enchanced when an IABP is positioned in the ascending aorta during urgent surgical revascularization.

Ventricular Defibrillation in Canines with Chronic Infarction, and Effects of Lidocaine and Procainamide

Prior studies in dogs with normal hearts have demonstrated that lidocaine increases but procainamide does not change the energy required for successful defibrillation. Because many postinfarct patients receiving implantable cardioverter defibrillator devices require adjunctive antiarrhythmic therapy, we have studied the effects of lidocaine and procainamide on the relationship between delivered voltage and defibrillation success in mongrel dogs 21 +/- 3 days following ligation of the left anterior descending and first diagonal coronary arteries. Internal defibrillation testing using a patch-patch electrode configuration was performed before and during the administration of saline controls (n = 10), lidocaine (n = 10) and procainamide (n = 10). The mean infarct size as determined by staining with tetrazolium was 13.4% +/- 8.3% of right and left ventricles, and did not differ significantly between groups. The 50% effective defibrillation (ED50) voltage increased with infusions of saline (16% +/- 15%), lidocaine (40% +/- 22%), and procainamide (13% +/- 15%) and the ED50 energy increased 41% +/- 44%, 104% +/- 62%, and 35% +/- 36%, respectively. However, the increase in ED50 voltages and energies were significantly greater in animals receiving lidocaine compared to those receiving either saline control or procainamide (P < 0.01). There were trends toward change of hemodynamic parameters in all animals following baseline defibrillation testing; stroke volume declined 21% +/- 16%; and mean pulmonary artery and aortic pressure increased by 22% +/- 25% and 11% +/- 15%, respectively. In conclusion, unlike our previous studies in dogs with normal hearts, in this model hemodynamic deterioration occurred with repeated fibrillation and defibrillation, and defibrillation voltage requirements increased in the control series. Taking into consideration the increase in defibrillation voltage requirements over the duration of the experiments, lidocaine increases and procainamide does not change ED50; thus, their effects are similar in normal and infarcted canine hearts.

Late potentials in an ovine model of acute transmural myocardial infarction.

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.

Experimental model of left ventricular failure

A model of chronic cardiac failure has undergone extensive hemodynamic investigation. Under anesthesia the homonymous and second diagonal coronary arteries of sheep have been ligated. The resulting myocardial infarction caused significant acute hemodynamic impairment (paired two-tailed t tests), mean pulmonary artery pressure increasing from 7.31 ± 0.94 to 13.80 ± 1.19 mm Hg ( p < 0.001), pulmonary artery diastolic pressure increasing from 4.94 ± 1.03 to 11.13 ± 1.27 mm Hg ( p < 0.001), and directly measured left ventricular enddiastolic pressure increasing from 9.31 ± 1.52 to 17.42 ± 1.82 mm Hg ( p < 0.001) after infarction documented with invasive monitoring. There was a hemodynamically significant left ventricular aneurysm (paired two-tailed t tests) in animals studied 3 months later, with increased mean pulmonary artery pressure from 7.20 ± 1.15 to 13.80 ± 2.00 mm Hg ( p = 0.009), an increase in pulmonary artery diastolic pressure from 4.60 ± 1.30 to 12.10 ± 2.06 mm Hg ( p = 0.006), and an increase in left ventricular end-diastolic pressure from 11.00 ± 1.94 mm Hg before infarction to 17.00 ± 2.69 mm Hg ( p = 0.038). We conclude that this is a useful model of chronic left ventricular failure that is reproducible and applicable to investigations of therapeutic options in chronic heart failure.

Large animal model of left ventricular aneurysm

In 28 Dorsett sheep, ligation of the distal homonymous (equivalent to human left anterior descending) and second diagonal coronary arteries produced a constant transmural infarct of 22.9% ± 2.5% (mean ± standard deviation) of the left ventricular mass. Serial left ventriculograms showed that within four hours the infarct segment expands, wall thickness decreases, and aceurysmal dilalation occurs and progresses over the next 60 days in all sheep. Epicardial ventricular point references indicated that adjacent noninfarcted myocardium participates in the formation of the aneurysm. Anatomy of the coronary vasculature was studied in 22 excised sheep hearts. In sheep, coronary arterial anatomy is remarkably constant. The left coronary artery provides all of the blood supply to the left ventricle and septum and only a small rim of both the anterior and posterior right ventricles. Crdiac veins from the left ventricle drain into the coronary sinus, which also receives the left azygos vein. Right ventricular veins drain separately. The essentially separate coronary circulations to the two ventricles, the paucity of coronary collateral circulation, and the consistent evolution of left ventricular infants into aneurysms are important advantages of the ovine model for both metabolic and ventricular maechanical studies of acute myocardial infarction and left ventricular aneurysm.

Resection of left ventricular aneurysm during hypothermic fibrillatory arrest without aortic occlusion

From December, 1977, through September, 1984, 100 consecutive patients had ventricular aneurysmectomy during hypothermic fibrillatory arrest without aortic occlusion. In the series were 83 men and 17 women, mean age 57.2 years. Primary indications for operation were angina pectoris in 42 patients, congestive heart failure in 23, angina plus congestive failure in 22, and refractory ventricular irritability in 13. Emergency operation was required for 13 patients with an intra-aortic balloon pump. Mean New York Heart Association Class was 3.1. Mean left ventricular end-diastolic pressure was 19.5 mm Hg, and mean left ventricular ejection fraction was 0.37. Concomitant coronary artery grafting was performed in 97 patients (mean 3.2 grafts/patient). Pressor agents were used in 21 patients and an intra-aortic balloon pump in two patients. Perioperative myocardial infarction was documented in one patient (1%). There were two hospital deaths (2%), both in patients with refractory ventricular irritability. At late follow-up (mean 38.5 months), 13 additional patients (13.3%) had died. Actuarial survival rate at 73 months was 77.0%. Survival rate was better for 93 patients with anterior aneurysms if the left anterior descending and/or diagonal coronary arteries were grafted with aneurysmectomy (p less than 0.03). Although only ventricular arrhythmias predicted early death (p less than 0.03), ejection fraction (p less than 0.01) and ventricular arrhythmias (p = 0.03) predicted late death. Ventricular aneurysmectomy during hypothermic fibrillatory arrest without aortic occlusion can be performed with low hospital mortality and good long-term results. When possible, left anterior descending and/or diagonal coronary arteries should be grafted when anterior aneurysms are resected.

Initial Experience With Sequential Internal Mammary Artery Bypass Grafts to the Left Anterior Descending and Left Anterior Descending Diagonal Coronary Arteries

Early patency and late patency have consistently been better with single internal mammary artery grafts than with saphenous vein conduits. To determine the efficacy of these two types of grafts in sequential anastomoses, we performed sequential anastomoses of the left internal mammary artery to the left anterior descending and diagonal coronary arteries in 40 patients and compared the results with those in 58 patients who received sequential saphenous vein grafts. Treatment with dipyridamole (starting 48 hours before operation) and aspirin (added 7 hours after operation) was given to the 40 patients with internal mammary artery grafts and to 32 of the 58 patients in the saphenous vein group. After the bypass procedure, mean blood flows were as follows: 68 ml/min in patients with internal mammary artery grafts, 73 ml/min in patients who received saphenous vein grafts and a placebo, and 99 ml/min in those who received saphenous vein grafts, aspirin, and dipyridamole. Early patency of sequential internal mammary artery grafts to the diagonal and left anterior descending coronary arteries was comparable to that of sequential saphenous vein grafts. Because a substantial late reduction in patency has been noted in sequential saphenous vein grafts, sequential internal mammary artery grafts may be the preferred conduit for coronary artery revascularization.

Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1 2 hours , disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK thearpy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.

Congenital Coronary Aneurysms Nine Years Following Saphenous Vein Bypass Graft Surgery

A 34-year-old woman with two congenital coronary aneurysms received a saphenous vein bypass graft (SVBG) as treatment for a thrombosed right coronary artery aneurysm 9 years ago. The angiographic and surgical findings were reported at that time [1]. In 1979, she received a sequential SVBG to the left anterior descending and first diagonal coronary arteries following recurrence of angina and progressive occlusion of the left coronary artery aneurysm. She is believed to have the longest angiographically documented course following operation, and her case history is reported to aid in establishing the natural history of this unusual condition and its surgical management.

Thermal quantification of region myocardial perfusion and heat generation

A technique for experimental determination of regional myocardial blood flow and heat generation has been developed, based on a heat-clearance method. This method allows repetitive and frequent measurements of regional blood flow without necessity for biopsy or microspheres. Testing was performed on a pedicle preparation, an intact segment of left ventricular myocardium dependent on a single diagonal coronary artery and situated in situ in the left ventricular free wall. Total blood flow to the pedicle was measured by an electromagnetic flow probe. A specially designed 3-thermistor microprobe was positioned in the pedicle to continuously sense temperature changes in the subepicardium, midmyocardium, and subendocardium. The theory underlying this method is based on a heat balance that includes local myocardial heating, conduction, and convection. Comparison of the predicted time- and position-dependent temperature with that measured experimentally allows extraction of the local myocardial blood flow and heating rates. This method allows resolution of differential flows in subendocardial, midmyocardial, and subepicardial myocardium and provides quantification of dynamic flow changes in each layer in response to various stimuli such as ischemia or pressor agents, without in itself causing damage to the myocardial microvasculature. Our data show total flow, based on summation of thermally calculated regional flows, to have correlation coefficients of 0.88 with both the flowmeter and microsphere results. Resting flow values for Nembutal-anaesthetized, open-chest dogs of 0.66 ml/(g . min) compare favorably with values obtained by microsphere studies. Infusion of norepinephrine increased total flow and all layer flows, but the increase in subendocardial flow with norepinephrine was less than the increase of the other layers, perhaps accounting for the vulnerability of this region during catecholamine stress. Local myocardial heating rates in subepicardial, midendocardial, and subendocardial layers are shown to follow the same dependence on local myocardial blood flow in response to anoxic stress or norepinephrine-induced vasodilation. Specifically, local heating rate increases to a factor of 10 at flow below resting level.

Two and three dimensional display of myocardial ischemic “border zone” in dogs

It is intuitively apparent that the ultimate fate of reversibly damaged, peri-ischemic “border zone” tissue should relate to individual patient survival. The purpose of this study was: (1) to describe a technique of assessing the adequacy of epicardial and myocardial oxygenation, and (2) to examine the extent and character of the peri-ischemic “border zone” in the dog after coronary arterial ligation. A diagonal branch of the left anterior descending coronary artery was ligated in four anesthetized open chest, neurohormonally intact dogs. The same diagonal coronary artery was ligated in six isolated perfused canine heart preparations in which coronary partial pressures of oxygen and carbon dioxide, pH, blood flow and temperature were fixed. The ischemic zones were rapidly frozen and reduced nicotinamide adenine dinucleotide (NADH) fluorescence photographs were taken of the epicardium and at 0.5 mm depths into the myocardium. The distinction between perfused and ischemic myocardium is not apparent with the naked eye or natural light photography. Epicardial and myocardial oxidation-reduction status is well seen with NADH fluorophotography. In both the intact and perfused heart preparations the NADH-fluorescent (ischemic) border is jagged along all edges. Islands of perfused nonfluorescent tissue appear within the ischemic border. The transition between NADH-fluorescent ischemic cells and adjacent nonfluorescent tissue is less than 0.1 mm. The ischemic border is narrow. The distance between homogeneously NADH-fluorescent tissue and homogeneously nonfluorescent tissue (across the zone of island normoxia or microheterogeneity) may be as wide as 6 to 8 mm.

Results of combined coronary endarterectomy and coronary bypass for diffuse coronary artery disease

The treatment of diffuse distal coronary artery disease is presently unsatisfying. Coronary artery bypass grafting (CABG) is usually not successful in these circumstances. Mechanical endarterectomy of a distal coronary artery combined with coronary artery bypass grafting (E-CABG) has been performed 26 times at this institution. Follow-up catheterization 6 months after operation revealed that 14 of the first 20 grafts studied were patent (70 percent). Twenty endarterectomies were performed to the distal right coronary artery, three to the distal left anterior descending coronary artery, two to the circumflex / obtuse marginal arteries, and one to the first diagonal coronary artery. The average flow in these patent grafts at the time of operation was 87 ml. per minute (range 30 to 200 ml. per minute). Intraoperatively, the six nonpatent grafts had flows averaging 27 ml. per minute. All of these patients had concomitant CABG's without endarterectomy to other coronary arteries. There were two perioperative myocardial infarctions. There were no early or late deaths. A literature survey shows that 605 CABG's constructed to endarterectomized coronary arteries have undergone postoperative catheterization. Four hundred seventy-seven (79 percent) of these E-CABG's were patent from 3 weeks to 2 years following operation. Histologic studies demonstrate that a neointima is formed over the endarterectomized surface. Neither thrombosis nor the recurrence of atherosclerosis seems to be the problem that many have feared. The present series, as well as the combined series from the literature, lends encouraging support to the value of E-CABG for the treatment of a diffusely diseased distal coronary artery.