Distal Left Circumflex Research Articles

A novel heart failure model induced by sequential coronary artery occlusions and tachycardiac stress in awake pigs

A heart failure model was developed using conscious pigs subjected to serial myocardial infarctions followed by intermittent rapid ventricular pacing. Aortic and atrial catheters, left ventricular (LV) pressure gauge, LV dimension crystals, ascending aortic flow probe, pacing leads, and two coronary artery occluders were implanted in 15 pigs. The initial distal left circumflex coronary artery (LCX) occlusion produced a modest infarct, i.e., 18 +/- 3% of LV, and the second proximal LCX occlusion, performed 48 h later, enlarged the infarct to 33 +/- 2% of the LV with only modest changes in LV function. Thereafter, the pigs were subjected to ventricular pacing at 220 beats/min, which was maintained for 7 days and terminated for 3 days. This pacing cycle was repeated two more times and resulted in significantly impaired LV function and systemic hemodynamics. For example, after the second cycle of pacing, LV rate of pressure change (dP/dt, -41 +/- 4% from 2,778 +/- 112 mmHg/s), velocity of circumferential fiber shortening (V(cf): -53 +/- 6% from 1.1 +/- 0.1 s(-1)), and cardiac index (CI: -42 +/- 5% from 122 +/- 4 ml. min(-1). kg(-1)) were reduced significantly, whereas LV end-diastolic diameter (EDD: +34 +/- 6% from 39 +/- 2 mm), total peripheral resistance (TPR: +75 +/- 16% from 0.79 +/- 0.05 U), and mean left atrial pressure (LAP) (+21 +/- 1 mmHg from 5 +/- 1 mmHg) were increased significantly. Importantly, 3 wk after cessation of the final pacing cycle, LV dP/dt (-40 +/- 5%), V(cf) (-48 +/- 9%), and CI (-30 +/- 4%) remained depressed, whereas LV EDD (+39 +/- 5%), TPR (+43 +/- 9%), and LAP (+13 +/- 4 mmHg) were still increased. In contrast, hemodynamic impairment in six conscious pigs subjected to pacing only did not persist when pacing was terminated. Thus this model could provide a unique opportunity to study both the effects of preclinical therapeutic interventions and the mechanisms involved in the development of heart failure.

Cambios de diámetro de las arterias coronarias en receptores de trasplante cardíaco con vasos angiográficamente normales durante cinco años

Diffuse or focal coronary artery narrowing is a frequent complication of cardiac transplantation. Coronary enlargement has also been described although it is less known. To study the changes of the coronary arteries in transplant recipients, we have performed a quantitative study throughout 5 years. Serial coronary angiography was performed annually in all survivors of heart transplant. Forty four patients with visually normal coronary arteries and at least 5 years of evolution were selected for this study. Quantitative measurements of the diameter of the coronary arteries were performed in each angiogram at different levels: proximal, medium and distal left anterior descending coronary artery; proximal and distal left circumflex; proximal, medium and distal right coronary artery. Changes in diameter were compared throughout the 5 years. In the entire group of patients there was a small increase in the diameter of each segment. Taking each patient separately, an enlargement of the diameter of the proximal descending coronary artery was seen in 17 cases; medium descending coronary artery in 13; distal descending coronary artery in 8; proximal left circumflex in 11; distal left circumflex in 14; proximal right coronary artery in 18; medium right coronary artery in 18 and distal right coronary artery in 15. In total, 114 of 352 coronary segments (32%) underwent dilatation. Only 6 patients failed to have dilatation of any segment. Enlargement of the coronary arterial diameter was seen in 32% of segments of the main coronary arteries in heart transplant recipients with angiographically normal coronary arteries during 5 years of evolution. This could be due to intimal thickening with overcompensation by an additional vessel enlargement with net lumen gain.

Woven left coronary artery disease

CASE 1. S.L., a 60-year-old patient, developed angina pectons and had a positive thalhum scan. Coronary ang~ograms showed apparently normal left mam trunk and proximal left anterior descending artery (LAD). Subsequently, the LAD subdivided into 3 channels, intertwining along their course. The diameter of the distal branches was small (Figure 1); consequently, we could not assess anglographically whether the branches fused again. The proximal left circumflex artery sutxtivlded into 2 channels that fused again along the mid-left circumflex artery. The d~stal obtuse marginal and the distal left circumflex artery showed a morphology w~th no angiographic evidence for reanastomosis CASE 2: T.G, a 62,year-old man, had ang~ography for angina after acute myocardial mfarcuon angina. The left coronary anglograms showed 85% stenosls of the m~dLAD. The left circumflex artery subdivided into 2 woven channels that fused again (Figure 2). A 50%

Endogenous adenosine and coronary vasoconstriction in hypoperfused myocardium during exercise

The coronary circulation has been shown to remain responsive to vasodilator and vasoconstrictor stimuli during myocardial ischaemia. The aim of this study was to investigate whether endogenous adenosine attenuates coronary vasoconstriction caused by the thromboxane A2 analogue, U46619. Nine chronically instrumented dogs were studied during treadmill exercise in the presence of a coronary stenosis which resulted in distal left circumflex coronary artery hypoperfusion. Myocardial blood flow was assessed with radioactive microspheres during exercise prior to and during intracoronary infusion of U46619 (0.01 microgram.kg-1 x min-1), in the absence and the presence of adenosine receptor blockade with intravenous 8-phenyltheophylline (5 mg.kg-1) and intracoronary adenosine deaminase (50 units.kg-1). Distal coronary pressure was maintained constant during the control stenosis and the three interventions, at 49(SEM 3), 50(3), 50(3), and 50(3) mm Hg. During control exercise mean myocardial blood flow was 0.91(0.09) ml.min-1 x g-1 in the stenosis region and 2.54(0.28) in the normal region. With no change in distal coronary pressure, U46619 decreased mean myocardial blood flow to 0.70(0.10) ml.min-1 x g-1 (p < 0.05). Adenosine blockade alone decreased myocardial blood flow in the stenosis region to 0.60(0.07) ml.min-1 x g-1 (p < 0.05 v control stenosis), indicating that endogenous adenosine contributed to coronary vasodilatation in the ischaemic region. However, adenosine blockade did not augment the vasoconstriction in response to U46619 [mean myocardial blood flow 0.49(0.05) ml.min-1 x g-1], indicating that endogenous adenosine did not attenuate the vasoconstriction caused by U46619. Endogenous adenosine contributed to dilatation of resistance vessels in hypoperfused myocardium of exercising dogs in the absence as well as in the presence of U46619. However, endogenous adenosine did not attenuate the magnitude of the vasoconstrictor response to U46619. These findings are best explained by observations that thromboxane A2 and adenosine act on coronary vascular segments of different size.

Serotonin selectively aggravates subendocardial ischemia distal to a coronary artery stenosis during exercise.

The coronary circulation has been shown to remain responsive to vasodilator and vasoconstrictor stimuli during myocardial ischemia. Because serotonin possesses both vasodilator and vasoconstrictor properties, we examined its effect in the coronary circulation distal to an arterial stenosis that resulted in myocardial hypoperfusion during exercise. Seven chronically instrumented dogs were studied during treadmill exercise in the presence of a stenosis that reduced distal left circumflex coronary artery perfusion pressure to 42 +/- 1 mm Hg. Myocardial blood flow was assessed with radioactive microspheres during exercise before and during intracoronary infusion of 0.4 and 2.0 micrograms/kg-1.min-1 serotonin. The stenosis was adjusted to maintain distal coronary pressure constant during control exercise and with the two doses of serotonin. In seven dogs, the effect of serotonin (2.0 micrograms/kg-1.min-1) was also studied during exercise with normal arterial inflow. During control exercise, the stenosis decreased mean myocardial blood flow to 45% of flow in the normally perfused region. This decrease was most pronounced in the subendocardium (endocardial/epicardial ratio 0.36 +/- 0.06 versus 1.46 +/- 0.14 in the control region; p < 0.01). With no change in pressure distal to the stenosis, serotonin decreased subendocardial flow from 0.51 +/- 0.09 ml/min-1.g-1 to 0.41 +/- 0.12 (p < 0.05) and then to 0.35 +/- 0.08 ml/min-1.g-1 (p < 0.05) and tended to increase subepicardial flow from 1.47 +/- 0.17 to 1.91 +/- 0.23 and 1.85 +/- 0.21 ml/min-1.g-1 (p = 0.08) during infusions of 0.5 and 2.0 micrograms/kg-1.min-1, respectively, with no change in total arterial inflow. In contrast, in the absence of a stenosis, serotonin (2.0 micrograms/kg-1.min-1) increased subendocardial flow from 2.43 +/- 0.25 to 3.73 +/- 0.25 ml/min-1.g-1 (p < 0.01) and subepicardial flow from 1.88 +/- 0.20 to 5.29 +/- 0.38 ml/min-1.g-1 (p < 0.01). During normal arterial inflow, serotonin dilated coronary resistance vessels and increased flow to all myocardial layers. During hypoperfusion, a vasodilator response was still present in the subepicardium, but vasoconstriction was then observed in the subendocardium. Our data suggest that serotonin constricts the intramural penetrating arteries, thereby selectively increasing resistance to subendocardial blood flow.

Coronary vasodilator reserve in ischemic myocardium of the exercising dog.

Previous work has reported that coronary vasodilator reserve may persist in myocardium rendered ischemic by hypoperfusion. This study investigated the presence and extent of residual coronary vasomotor tone in myocardial regions made acutely ischemic by a flow-limiting coronary stenosis during exercise. Studies were done in chronically instrumented dogs undergoing treadmill exercise in the presence of a coronary stenosis that decreased distal left circumflex coronary artery perfusion pressure to approximately 40 mm Hg. Measurements of myocardial blood flow were made with radioactive microspheres during exercise (6.5 km/hr, 6% grade) before and during intracoronary infusion of the potent coronary vasodilator adenosine (40 micrograms/kg/min). Distal coronary perfusion pressure was held equal before and during intracoronary adenosine infusion (43 +/- 5 versus 42 +/- 5 mm Hg) by adjusting the hydraulic coronary occluder. During exercise in the presence of a coronary stenosis, myocardial blood flow (milliliter per minute per gram) was significantly reduced in all layers of the ischemic posterior region compared with the nonischemic anterior region. During intracoronary adenosine infusion, with no change in coronary perfusion pressure, myocardial blood flow was significantly increased compared with preadenosine flows for both the subendocardial layer flow (1.03 +/- 0.74 versus 0.66 +/- 0.50; p less than 0.05) and mean transmural flow (1.54 +/- 0.59 versus 1.16 +/- 0.36; p less than 0.05). In the presence of a coronary stenosis, regional myocardial segment shortening in the ischemic region during exercise fell significantly to 49 +/- 8% of shortening in the absence of a coronary stenosis but improved modestly during adenosine infusion (65 +/- 7 versus 49 +/- 8%; p less than 0.05). These results indicate that adenosine-responsive coronary vasodilator reserve persists during exercise-induced myocardial ischemia and suggest that residual microvascular vasoconstrictor tone may affect the extent of myocardial hypoperfusion occurring consequent to a flow-limiting coronary stenosis.

Right coronary artery originating from distal left circumflex: an unusual feature of single coronary artery

This report describes a patient with a single coronary artery system, in whom the right coronary artery originated from the distal left circumflex. A significant stenosis was present just at the take-off of the aberrant right coronary artery. No other associated cardiac anomaly could be demonstrated; the patient was referred for elective bypass surgery.

Xamoterol recruits an inotropic reserve in the acutely failing, reperfused canine myocardium without detrimental effects on its subsequent recovery

The present study tested (1) whether xamoterol recruits an inotropic reserve in reperfused myocardium and (2) whether acute inotropic stimulation by xamoterol has deleterious consequences on the long-term recovery of the reperfused myocardium. Sixteen anaesthetized, open-chest dogs were bilaterally vagotomized and heart rate kept constant by left atrial pacing. The distal left circumflex coronary artery was occluded for 15 min and then reperfused for 8 h. The coronary occlusion resulted in regional myocardial dyskinesia and myocardial function remained severely depressed after release of the occlusion. At 10 min reperfusion, 8 dogs received xamoterol (100 micrograms/kg i.v.), whereas the remaining 8 dogs served as controls and received saline. Xamoterol increased mean systolic wall thickening velocity (from 1.47 +/- 2.34 (SD) mm/s at 10 min reperfusion to 7.13 +/- 3.55 mm/s at 30 min reperfusion and 7.64 +/- 2.48 mm/s at 1 h reperfusion, respectively, both P less than 0.05). In the control group, only a slow recovery of mean systolic wall thickening velocity was observed (from 3.14 +/- 3.30 mm/s to 2.96 +/- 3.74 mm/s and 4.03 +/- 3.00 mm/s at 10 min, 30 min, and 1 h reperfusion, respectively). At 8 h reperfusion, mean systolic wall thickening velocity was similar in both groups (7.97 +/- 4.23 mm/s in the xamoterol-group and 6.87 +/- 4.00 mm/s in the placebo-group). Histological examination revealed no difference in the extent of necrosis between the two groups after 8 h reperfusion. We conclude that (1) xamoterol recruits an inotropic reserve in reperfused myocardium, and (2) this recruitment of an inotropic reserve does not compromise functional recovery and structural integrity of the reperfused myocardium.

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics in humans.

Effects of H1-receptor stimulation on coronary arterial diameter and coronary hemodynamics were examined in 11 patients with angiographically normal coronary arteries and without variant angina or resting angina. Selective H1-receptor stimulation was achieved by infusing histamine into the left coronary artery at a rate of 2.0 micrograms/min for 5 minutes after pretreatment with cimetidine (25 mg/kg). Plasma histamine concentration in the coronary sinus, coronary sinus blood flow, heart rate, and aortic pressure were measured before, during, and after the histamine infusion. Coronary arterial diameter was measured by cinevideodensitometric analysis of coronary arteriograms performed before and immediately after the histamine infusion. During the histamine infusion, plasma histamine concentration in the coronary sinus increased from 0.33 +/- 0.06 to 5.86 +/- 0.71 ng/ml (p less than 0.01); coronary sinus blood flow increased from 98 +/- 12 to 124 +/- 13 ml/min (p less than 0.01), and coronary vascular resistance decreased from 1,113 +/- 117 to 851 +/- 91 mm Hg.min/l (p less than 0.01). Heart rate and aortic pressure remained unchanged. The mean luminal diameters of the proximal, middle, and distal left anterior descending artery increased by 9.4 +/- 3.6% (p less than 0.05), 19.2 +/- 3.8% (p less than 0.001), and 31.5 +/- 5.6% (p less than 0.001), respectively, after the histamine infusion. The mean luminal diameters of the proximal, middle, and distal left circumflex artery increased by 15.2 +/- 3.6% (p less than 0.01), 17.5 +/- 5.2% (p less than 0.01), and 20.6 +/- 4.3% (p less than 0.001), respectively, after the histamine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Essential fatty acid deficiency inhibits early but not late leukocyte infiltration in rabbit myocardial infarcts

Essential fatty acid (EFA) deficiency, induced by elimination of the dietary (n-6) fatty acids, has been shown to limit inflammatory cel influx and consequent enhanced eicosanoid production in experimental glomerulonephritis and hydronephresis. To determined whether EFA-deficiency exerts anti-inflammatory efects following left ventricular myocardial infarction (LVMI), male weanling rabbits were fed EFA-deficient diet for 3 months prior to 60 minutes of distal left circumflex coronary artery occlusion followed by reperfusion. One and 4 days later, corresponding to infiltration of cardiac tissue with polymorphonuclear (PMN) and mononuclear leukocytes respectively, infarcted hearts were buffer perfused and stimulated to produced eicosanoids with f-met-leu-phe or bradykinin. One day following LVMI, the hearts of EFA-deficient rabbits demonstrted a marked suppression of PMN infiltration and eicosanoid production relative to controls. Four days following myocardial infarction, no differences were obseved in mononuclear cell invasion, collagen deposition, or eicosanoid production between EFA-deficient and normal hearts. Our data show that EFA-deficiency inhibits PMN influx and consequent enhanced eicosanoid production without affecting the later appearance of mononuclear cells, collage deposition, or eicosanoid production. Recent studies have shown that suppression of PMN invasion limits the extent of tissue damage following LVMI. Selective inhibition of PMN infiltraton is possible and may be useful in the management of acute myocardial infarction.

Value of the ST-T segment in lead V4R in inferior wall acute myocardial infarction to predict the site of coronary arterial occlusion

The treatment of acute myocardial infarction (AMI) has changed dramatically with the introduction of thrombolytic therapy, immediate angioplasty and emergency coronary artery bypass surgery. Several studies1e3 have shown that the success rate of these procedures depends on the time interval between the onset of complaints and the achievement of reperfusion. In patients admitted with an inferior wall AMI, the coronary artery causing the AM1 can be the right or the left circumflex artery. Our previous investigations, as well as those of others,4-6 have shown that the recording of lead V4R in the acute phase of an inferior wall AM1 can distinguish those patients with a proximal occlusion of the right coronary artery from those with an occlusion of the distal right or left circumflex artery, the first group of patients showing ST-T-segment elevation I1 mm in lead V4R. However, it is not possible to differentiate between occlusion of a distal right coronary artery and a circumflex artery using this criterion. In these patients (possible candidates for intracoronary thrombolytic therapy), coronary arteriography might start with the “wrong” coronary artery leading to a delay in reperfusion. Retrospectively, we have analyzed the configuration of the ST-T segment in lead V4R to determine if changes in the ST-T segment can help predict the site of coronary occlusion in inferior wall AMI.

Digital fluoroscopy and intravenous cardiac angiography for the detection of coronary artery disease in selected subjects. A feasibility study.

Thirty-seven thin patients (height/weight ratio >2.2 cm/kg) without prior myocardial infarction underwent digital subtraction fluoroscopy and intravenous digital subtraction cardiac angiography one day before they were scheduled to undergo coronary angiography. Eighteen (49%) had at least a 50% obstruction of a major coronary artery as shown on selective coronary cineangiograms; eight of these (44%) had three calcified coronary arteries as visualized by digital fluoroscopy, five (28%) had diagnostic wall-motion abnormality by digital ventriculography, and 15 (83%) had intravenous angiographic evidence of at least one severe (>50%) coronary obstruction. Seventeen (94%) of the 18 with severe selective angiographic obstructions had at least one calcified artery detected by the digital study. Seventeen (89%) of the 19 without angiographic evidence of severe disease had none of these three abnormalities visualized on their digital intravenous images. Intravenous cardiac angiography was more accurate for predicting proximal coronary, right coronary, and left anterior descending branch obstructions, than for distal coronary and left circumflex artery obstructions.

Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of intracoronary injection of acetylcholine on coronary arterial diameter

The effects of intracoronary injection of acetylcholine on coronary arterial diameter was examined by coronary arteriography in 30 adult patients (13 men, 17 women), aged 23 to 67 years (mean 51), with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and other severe cardiac diseases were excluded. Two minutes after injection of 30 to 100 μg of acetylcholine into the left coronary artery, significant diffuse narrowing (more than 25% reduction in diameter) of the left main trunk, the proximal, mid- and distal left anterior descending artery, and the proximal, mid- and distal left circumflex artery occurred in 1 (4%), 5 (20%), 3 (12%), 9 (36%), 6 (24%), 8 (32%) and 3 (12%) of 25 patients, respectively. After injection of 30 to 50 μg of acetylcholine into the right coronary artery, significant diffuse narrowing of the proximal, mid- and distal right coronary artery occurred in 5 (25%), 7 (35%) and 10 (50%) of 20 patients, respectively. However, significant diffuse dilatation (more than 25% increment in diameter) appeared in the left main trunk, left anterior descending, left circumflex and right coronary arteries in a few patients. These results indicate that acetylcholine induces coronary vasoconstriction in a significant number and coronary vasodilatation in a small number of adult humans, and that response of the coronary artery to acetylcholine varies along the course of the coronary artery.

Effects of nitroglycerin-induced hypotension on myocardial blood flow in a two vessel occlusion-stenosis anesthetized canine model

The effects of acute occlusion of the left anterior descending coronary artery on regional blood flow (microspheres) to the remote bed supplied by either an unstenosed or a stenosed circumflex coronary artery were assessed during the infusion of intravenous nitroglycerin in 11 open chest barbiturate-anesthetized mongrel dogs. Left anterior descending coronary artery occlusion in the presence of an unstenosed left circumflex artery during nitroglycerin infusion caused systolic aortic and distal circumflex pressure to decrease significantly from 98 +/- 4 to 91 +/- 3 and from 99 +/- 4 to 92 +/- 3 mm Hg, respectively. Remote circumflex bed flow was unchanged. The infusion of intravenous nitroglycerin in the presence of a left circumflex stenosis (gradient 31 +/- 3 mm Hg) reduced systolic aortic and distal circumflex pressure to 98 +/- 2 (p = 0.001) and 71 +/- 4 mm Hg (p = 0.001), respectively, and lowered remote circumflex bed endocardial flow from 1.00 +/- 0.08 to 0.79 +/- 0.07 ml/min per g (p = 0.001). When the left anterior descending coronary artery was occluded under these conditions, systolic aortic and distal left circumflex pressure decreased to 89 +/- 3 (p = 0.005) and 62 +/- 4 mm Hg (p = 0.08), respectively. Remote circumflex artery bed endocardial and transmural flow were significantly reduced to 0.58 +/- 0.07 (p = 0.01) and 0.65 +/- 0.07 ml/min per g (p = 0.03), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Catecholamine release and ventricular arrhythmias during coronary occlusion and reperfusion in the dog.

In anesthetized dogs, 60-min occlusions of either the proximal (n = 14), distal (n = 8) left circumflex (LCX), or left anterior descending (LAD, n = 10) arteries were followed by reperfusion. Coronary sinus and aortic norepinephrine and epinephrine plasma concentrations were measured. The ventricular arrhythmias were ventricular premature depolarizations (VPDs), unsustained ventricular tachycardia (VT) (greater than or equal to 3 and less than 20 VPDs), sustained VT (greater than or equal to 20 VPDs), and ventricular fibrillation (VF). A gradual twofold increase (p less than 0.05) in myocardial norepinephrine overflow followed occlusion in all three groups. The increases in the amounts of norepinephrine released in the coronary sinus blood during reperfusion were significant and proportional to the size of the occluded area: proximal LCX, from 0.236 +/- 0.038 to 1.528 +/- 0.490 ng/mL of plasma (p less than 0.001); LAD, from 0.180 +/- 0.027 to 0.795 +/- 0.286 ng/mL (p less than 0.05); distal LCX, from 0.215 +/- 0.039 to 0.404 +/- 0.110 ng/mL (p less than 0.05). Aortic epinephrine concentrations were significantly increased only by LAD occlusion; at 15 min, the value had increased to 0.187 +/- 0.053 ng/mL from an initial value of 0.069 +/- 0.029 ng/mL (p less than 0.001). Two phases of ventricular arrhythmias followed both occlusion and reperfusion. Phase 1 postocclusion was characterized by VPDs and phase 2 by VPDs and unsustained VT. Sustained VT was seen only in phase 1 postreperfusion, whereas unsustained VT was seen in phase 2. VF was seen in 50, 35, and 25% of the dogs with proximal LCX, LAD, and distal LCX occlusion and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Origin of the left anterior descending coronary artery from the pulmonary artery: 3 year angiographic follow-up after saphenous vein bypass graft and proximal ligation

A 55 year old woman had an extremely rare congenital anomaly of the coronary circulation in which the left anterior descending coronary artery arose from the pulmonary artery. Proximal ligation and saphenous vein grafting to the aberrant vessel were performed. Five month and 3 year angiographic follow-up studies demonstrated 1) a widely patent vein graft, 2) regression of large collateral vessels between the right coronary and circumflex arteries and the left anterior descending artery, and 3) marked attenuation of the distal right coronary and left circumflex arteries on the 3 year study. This report describes the clinical course of the oldest reported patient with this unique coronary artery anomaly and the only angiographic study of the effect of ligation and saphenous bypass grafting on its natural history.

Beneficial effect of amrinone on myocardial oxygen consumption during acute left ventricular failure in dogs

In 11 dogs ischemic left ventricular failure characterized by a 30 percent reduction In cardiac output and a left ventricular end-dlastolic pressure of 18 mm Hg or more was produced by proximal occlusion of the left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. Administration of amrlnone In an Intravenous bolus injection followed by a constant Infusion produced Improvements in cardiac output (from 1.62 ± 0.50 to 2.19 ± 0.52 Itters/min [ mean ± standard deviation], p <0.05), left ventricular end-dlastolic pressure (from 21.6 ± 3.5 to 11.0 ± 5.4 mm Hg, p <0.05) and peak positive rate of rise of left ventricular pressure [dP/dt](from 1,264 ± 241 to 1,800 ± 458 mm Hg· −1, p <0.05). These Improvements were maintained throughout the 20 minute period of therapy. No significant alteration in heart rate or arterial pressure was noted. In parallel with the hemodynamic improvement myocardial oxygen consumption improved to 0.094 ± 0.05 and 0.092 ± 0.04 vol· −1⋗ −1 after 2 and 20 minutes; respectively, of amrinone compared with 0.124 ± 0.05 during left ventricular failure (both <0.05). The effects of amrinone on left ventricular failure are due to augmented contractility and mild systemic vasodllatation. The reduction in myocardial oxygen consumption during amrlnone-treated left ventricular failure presumably results from a reduction in ventricular wall tension that more than offsets the effect of an Increase in contractility.

Exercise can promote coronary collateral development without improving perfusion of ischemic myocardium.

We studied the effect of exercise training on the coronary collaterals that developed in response to gradual coronary occlusion in dogs. After their proximal left circumflex coronary artery occlusion, 33 dogs were randomly assigned to exercise or sedentary groups. Coronary collateral function was evaluted 5 weeks or 8 weeks later. The exercised dogs developed better epicardial collateral connections to the occluded left circumflex as judged by higher retrograde blood flow from the distal left circumflex and lower pressure drop across the collaterals. No difference in collaterals was apparent angiographically. Microsphere data indicated that exercise dogs were not better protected against tachycardia provoked subendocardial ischenia in the myocardium supplied by the collaterals.

Effect of extension of infarction on serial CK activity.

The effects of extension of myocardial infarction by reduction of regional myocardial blood flow (RMBF) to an ischemic region on serum CK activity was examined in 14 awake dogs. Initial infarction was effected by occlusion of the distal left circumflex coronary artery (LCCA) and subsequent extension was produced by occlusion of the proximal LCCA 6, 12 or 18 hours after distal occlusion. Extension was verified by serial measurements of RMBF using radioisotope-labeled microspheres before and after proximal occlusion. Serum CK activity increased initially 2-4 hours after distal coronary occlusion and then increased rapidly and reached peak values 12 hours after occlusion. When the infarction was extended at 6, 12 or 18 hours after initial occlusion, CK appearance was immediately reduced in the 6- and 12-hour experiments, but not in the 18-hour experiments. Extension of infarction at each interval caused delayed increases in CK activity beginning 2-5 hours after proximal occlusion, with peak values occurring 12 hours later. The immediate effects of extension of infarction by reducing blood flow on CK activity are a function of whether the infarcted myocardium continued to release CK, e.g., at 6 and 12 hours after occlusion, or CK release was completed, e.g., 18 hours. The immediate effects of extension of infarction were the result of perfusion on myocardium that is infarcted and continues to release CK, and do not necessarily indicate alterations in the extent of myocardial injury. The delayed effects of proximal and distal occlusion on CK activity were comparable, suggesting that delayed and not immediate alterations in CK activity represent extension of infarction.