Great Cardiac Vein Blood Research Articles

Myocardial ischemia-reperfusion damage after pacing-induced tachycardia in patients with cardiac syndrome X

The presence of myocardial ischemia in syndrome X (chest pain, "ischemia-like" electrocardiogram changes, and normal coronary angiograms) is uncertain possibly because, when focally distributed, it may not cause contractile dysfunction or lactate production. We measured lipid hydroperoxides (ROOHs) and conjugated dienes (CDs), two sensitive, independent markers of ischemia-reperfusion oxidative stress, in paired aortic and great cardiac vein blood samples before and after pacing-induced tachycardia in nine patients with syndrome X. Diagnostic ischemic S-T segment changes during pacing were followed by a consistent increase in ROOH and CD levels in the great cardiac vein (from 4.83 +/- 1.18 micromol/l at baseline to 7.88 +/- 1.12 micromol/l and from 0.038 +/- 0.002 to 0.051 +/- 0.003 arbitrary units, respectively, P < 0.01). In controls, ROOH and CD levels did not change after pacing. The large postpacing cardiac release of lipid peroxidation products, consistently observed in all patients and similar to that previously observed after ischemia caused by percutaneous transluminal coronary angioplasty, is consistent with an ischemic origin of syndrome X.

Role of Adenosine in Pathogenesis of Syndrome X: Assessment With Coronary Hemodynamic Measurements and Thallium-201 Myocardial Single-Photon Emission Computed Tomography

Objectives. This study was performed 1) to examine the role of adenosine in the pathogenesis of syndrome X in patients with this syndrome and abnormal results on myocardial scintigrams during exercise, and 2) to determine the susceptibility to myocardial ischemia in this subset of patients with syndrome X.Background. A role for adenosine in the pathogenesis of syndrome X has recently been postulated, but there are few clinical data supporting this hypothesis.Methods. Exercise thallium-201 myocardial scintigraphy after intravenous administration of aminophylline, an adenosine receptor blocking agent, or saline solution and adenosine thallium-201 scintigraphy were performed in 26 patients with syndrome X. Hemodynamic variables during exercise and perfusion defect size after aminophylline and saline infusions were compared. At cardiac catheterization, coronary hemodynamic variables during separate infusions of adenosine and dobutamine were also examined and were compared among patients with abnormal or normal scintigrams and 10 control subjects.Results. Perfusion abnormalities on exercise-thallium-201 scintigraphy occurred in 14 of 26 patients with syndrome X. Intravenous infusion of aminophylline suppressed the scintigraphic perfusion defect and prolonged the time to 1-mm ST segment depression in patients with syndrome X with abnormal exercise scintigrams. Intravenous infusion of adenosine induced a perfusion defect in the same myocardial area where the perfusion defect was observed at exercise in 7 of the 14 patients with syndrome X. At cardiac catheterization, patients with syndrome X with abnormal exercise scintigrams had lower coronary flow reserve and a greater frequency of myocardial lactate production and ST segment depression in response to the infusions of adenosine and dobutamine than did the other two groups. During adenosine infusion, great cardiac vein blood flow and oxygen content were significantly increased and myocardial oxygen consumption and lactate extraction were significantly reduced from baseline without a significant increase in rate-pressure product in this subset of patients with syndrome X.Conclusions. Patients with syndrome X with abnormal exercise scintigrams have high susceptibility to myocardial ischemia during exercise or pharmacologic stress tests, probably owing to reduced coronary flow reserve. A heterogeneous response to endogenous adenosine may contribute to scintigraphic perfusion abnormalities and myocardial ischemia during exercise in this subset of patients with syndrome X.

Inotropic stimulation by dobutamine increases left ventricular regional function at the expense of metabolism in hibernating myocardium

The mechanism by which dobutamine increases the contraction of chronically dysfunctional myocardium and its effects on metabolism are still unknown. The aim of this study was to assess regional myocardial metabolism at rest and during an intracoronary dobutamine infusion in patients with hibernating myocardium. Eleven asymptomatic patients with single proximal stenosis of the left anterior descending coronary artery and persistent left ventricular dysfunction at rest (undergoing percutaneous transluminal coronary angioplasty [PTCA]) were studied prospectively. Regional left ventricular function was assessed by two-dimensional (2D) echocardiography and regional perfusion by thallium-201 single-proton-emission computed tomography. Great cardiac vein and aortic blood samples were obtained for measurements of lactate and plasma free fatty acid (FFA) concentrations. Inotropic challenge, obtained by using intracoronary dobutamine infusion, increases regional left ventricular function. However, the arteriovenous AV lactate difference was 0.206 ± 0.070 mmol/L at rest, and it decreased to 0.018 ± 0.069 mmol/L ( p < 0.05 vs baseline) and 0.066 ± 0.068 mmol/L ( p < 0.05 vs baseline) at 4 and 10 minutes of dobutamine infusion, respectively. Thus the hibernating myocardium does not produce lactate at rest. However, when regional contraction is stimulated, dobutamine-induced inotropic challenge may cause a perfusion-contraction mismatch with an activation of anaerobic glycolysis.

Vasotonic angina: A spectrum of ischemic sysdroms involving function abnormalities of the epicardial and microvascular coronary circulation

Objectives. The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia.Background. Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous angina attacks or exercise stress testing.Methods. Twenty-five patients with no or minimal (<30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina).Results. Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 ± 4%) and those with coronary artery disease (5 ± 3%) but severe (p < 0.001) in those with variant angina (28 ± 14%) or syndrome × (25 ± 13%). Concomitant determination of coronary flow showed significant (p < 0.001) decreases in those with variant angina (25 ± 11%) and syndrome × (28 ± 10%) but not in control patients (5 ± 8%) or those with coronary artery disease (4 ± 5%), Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin.Conclusions. These indicate vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographicaily normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Comparison of isradipine with nitroprusside for control of blood pressure following myocardial revascularization: Effects on hemodynamics, cardiac metabolism, and coronary blood flow

The effects of isradipine (ISR) on cardiac performance, myocardial metabolism, and coronary blood flow were compared with those of sodium nitroprusside (SNP) when used to control blood pressure following myocardial revascularization. Twenty patients were randomized to receive either intravenous ISR or SNP if arterial blood pressure increased above 130 mm Hg systolic. Hemodynamic and metabolic parameters were studied using radial, pulmonary arterial, and coronary sinus catheters. Cardiac output and coronary blood flows were measured by thermodilution and blood was taken for calculation of myocardial oxygen consumption and lactate extraction. Electrocardiographic changes were recorded by Holter monitoring throughout the study. ISR and SNP both produced a satisfactory reduction in blood pressure accompanied by a decreased systemic vascular resistance ( P < 0.001). ISR infusion was associated with increases in cardiac output and stroke index ( P < 0.01), which were not apparent in the SNP group. Tachycardia occurred with SNP ( P < 0.01) but not with ISR therapy. Right and left ventricular stroke work indices and myocardial oxygen consumption were reduced with SNP. The ISR group showed unchanged myocardial oxygen consumption with increased right ventricular stroke work index. Coronary vascular resistance decreased ( P < 0.01) during ISR infusion but decreased only slightly in the SNP group. Great cardiac vein blood flow was significantly increased with ISR but not with SNP, resulting in a significant difference between the groups ( P < 0.05). Coronary sinus blood flow increased after control of blood pressure with ISR, whereas SNP was associated with a decrease in flow throughout the infusion period and one patient suffered myocardial ischemia during treatment. SNP caused reductions in mean pulmonary artery and right atrial pressures ( P < 0.05) as well as pulmonary vascular resistance ( P < 0.01), confirming SNP is a pulmonary vasodilator. Pulmonary vasodilatation was not a feature of ISR therapy. ISR appears to be a safe, effective alternative to SNP when used to control blood pressure following myocardial revascularization, and ultimately may prove to be superior.

Effects of atrial pacing and dipyridamole administration on coronary hemodynamics of collateralized myocardial regions in stable angina pectoris

Great cardiac vein blood flow by thermodilution and great cardiac vein oxygen saturation were measured in 14 patients with stable exertional angina and an angiographic pattern of complete occlusion of the proximal left anterior descending artery retrogradely filled by collateral vessels supplying still viable myocardium. Measurements were obtained under control conditions, at peak atrial pacing and after dipyridamole administration (0.56 mg/kg intravenously over 4 minutes). Both stress tests induced ischemic electrocardiographic changes in all patients, but dipyridamole administration resulted in greater ST-segment depression in 11 patients (1.6 ± 0.5 vs 2.4 ± 1.6 mm, p < 0.05) and transient ST-segment elevation in 3 patients. Dipyridamole provoked ischemia at a lower value of rate-pressure product (145.3 ± 30.6 vs 202.9 ± 36.6 beats/min · mm Hg · 10 −2, p < 0.0005) and anterior region myocardial oxygen consumption (9.32 ± 4.76 vs 11.39 ± 3.91 ml/min, p < 0.05), despite a greater increase in great cardiac vein flow (139.4 ± 45 vs 93 ± 27.4 ml/min, p < 0.0025) and a greater decrease in the calculated index of anterior region coronary resistance (0.87 ± 0.27 vs 1.46 ± 0.43 mm Hg/ml/min, p < 0.0005). Moreover, great cardiac vein oxygen saturation increased more significantly during dipyridamole-induced ischemia than at peak pacing (63 ± 12 vs 35 ± 8%, p < 0.0005). These data show that dipyridamole administration induces more profound electrocardiographic signs of myocardial ischemia than atrial pacing in patients with stable angina and an occluded left anterior descending artery retrogradely filled by collateral vessels. The vasodilation induced by the drug markedly exceeds that induced by pacing, despite lower values of myocardial oxygen consumption.

Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation.

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.

Incomplete global myocardial ischemia during cardiac arrest and resuscitation.

During cardiac arrest (no flow) and CPR (low flow), the onset of myocardial ischemia is followed by myocardial respiratory acidosis. Myocardial contractility is more decreased by respiratory than by metabolic acidosis. We demonstrated in a porcine model of cardiac arrest and in human patients increases in mixed venous PCO2 during CPR, whereas PaCO2 was decreased. Consequently, there was a striking increase in the venoarterial gradients for both [H+] and CO2. Both cardiac output (pulmonary blood flow) and the concentration of expired CO2 were simultaneously decreased. In great cardiac vein blood, even more profound respiratory acidosis with only minor decreases in bicarbonate and only moderate increases in lactate were observed. Intramyocardial pH was profoundly decreased. The severity of respiratory acidosis as a determinant of resuscitability and survival should be further investigated.

Global and Regional Myocardial Blood Flow and Metabolism during Equipotent Halothane and Isoflurane Anesthesia in Patients with Coronary Artery Disease

Global and regional myocardial blood flow and metabolism were examined in 20 patients with coronary artery disease before surgical stimulation. Half were anesthetized with halothane (0.8%) and half with isoflurane (1.2%). Coronary perfusion pressure decreased similarly in both groups. During halothane anesthesia coronary sinus blood flow, an index of global perfusion, decreased from an awake value of 129 +/- 7 to 97 +/- 7 ml/min (P less than 0.05), and great cardiac vein blood flow, an index of regional perfusion, decreased from 60 +/- 8 to 44 +/- 5 ml/min (P less than 0.05). In contrast, during isoflurane anesthesia global coronary blood flow increased from 131 +/- 13 to 153 +/- 16 ml/min (P less than 0.05), while regional blood flow decreased from 68 +/- 7 to 56 +/- 6 ml/min (P less than 0.05). Thus, the ratio of great cardiac vein blood flow to coronary sinus blood flow was unchanged during halothane anesthesia but decreased significantly during isoflurane. Neither global nor regional coronary vascular resistance was altered by halothane, whereas isoflurane decreased global coronary vascular resistance without affecting regional coronary vascular resistance. All patients receiving halothane had net myocardial lactate extraction. In the isoflurane group, four patients showed global lactate production and three regional lactate production. All patients demonstrating lactate production also developed electrocardiographic evidence of myocardial ischemia, which was not present before induction. The authors conclude that halothane is a preferable anesthetic to isoflurane in patients with coronary artery disease because the latter has the propensity to induce maldistribution of the coronary circulation and myocardial ischemia.

The Effects of Coronary Angioplasty on Nitroglycerin‐Induced Augmentation of Regional Myocardial Blood Flow

Percutaneous transluminal coronary angioplasty (PTCA) may improve coronary vasomotor responses after relief of flow limiting luminal narrowings. To evaluate the effects of PTCA on nitro‐glycerin‐induced augmentation of coronary blood flow, great cardiac vein (thermodilution) blood flow and systemic hemodynamic responses to low (50 meg) and high (200 meg) dose intracoronary nitroglycerin (NTG) before and after PTCA were measured in 20 patients undergoing left anterior descending artery (LAD) balloon dilatation. Before PTCA, low dose NTG increased great vein flow 44 ±31% (from 56 ± 21 to 81 ± 33 mL/min, P &lt; 0.01). High dose NTG increased great vein flow 55 + 30% (56 ± 23 to 87 ± 38 mL/min, P &lt; 0.01). PTCA reduced LAD stenosis (79 ± 13 to 20 ± 9%, P &lt; 0.01) and translesional pressure gradient (49 ± 10 to 15 ± 13 mmHg, P &lt; 0.01) increasing post‐PTCA basal great vein flow 45% (56 ± 21 mL/min to 81 ±27 mL/min, P &lt; 0.01).After PTCA, low dose NTG increased great vein flow only 26 ± 23% (81 ± 27 to 101 ± 39mL/min, P &lt; 0.01; P &lt; 0.05 versus 44 ± 31% before PTCA). The high dose NTG‐induced coronary hy‐peremic responses were unchanged after PTCA (55 ± 30, 55 ± 34%, P = ns). When compared to dose related NTG hyperemic responses in 10 patients with normal LAD, the post‐PTCA responses remained attenuated.These data indicate that NTG‐induced augmentation of coronary blood flow remains unchanged or attenuated and does not appear to be improved by PTCA. These findings should be considered when evaluating pharmacological coronary blood flow responses after PTCA. These data also suggest that epicardial coronary resistance plays a limited role in NTG‐induced augmentation of coronary blood flow inpatients with atherosclerotic coronary disease. (J Interven Cardiol 1988:1:2)

Intravenous nifedipine for control of hypertension in patients after coronary artery bypass graft surgery

A study was undertaken to assess the use of intravenous nifedipine in controlling hypertension in patients following coronary artery surgery. A combined hemodynamic and metabolic assessment was carried out in 15 patients on data recorded at six sequential time intervals: (1) baseline, (2) control of blood pressure, (3) 30 minutes after control of blood pressure, (4) 1.5 hours after control of blood pressure, (5) 3.5 hours after control of blood pressure, and (6) 30 minutes after discontinuing nifedipine. Coronary sinus and great cardiac vein blood flows were measured by the continuous thermodilution technique using the Baim coronary sinus flow catheter. Intravenous nifedipine was run initially at an average rate of 1.82 μg/kg/min. It took an average time of 12 minutes to lower the blood pressure to less than 130 mmHg systolic. There were highly significant decreases in systolic, mean, and diastolic blood pressures (P < .001), associated with significant decreases in systemic vascular resistance ( P < .001) and left ventricular stroke work index ( P < .05). There was an increase in cardiac output at 30 and 90 minutes of infusion (P < .05), and the stroke volume was increased 90 minutes after starting nifedipine (P < .05). The increase in heart rate was not significant. There was no significant effect on conduction times as measured by PR and QRS intervals on the ECG. However, the QTc interval was decreased after 3.5 hours (P < .05). There was an increase in right atrial pressure at 90 minutes and again 30 minutes after stopping nifedipine. (P < .05). The pulmonary artery pressure also was increased after stopping the infusion (P < .05). The pulmonary capillary wedge pressure, pulmonary vascular resistance, and right ventricular stroke work index remained unchanged. Coronary sinus and great cardiac vein flows were maintained despite a decrease in perfusion pressure, suggesting that nifedipine is a potent coronary vasodilator. Indeed, coronary vascular resistance was significantly decreased (P < .05). Myocardial oxygen consumption remained unchanged. The lactate extraction indicated that myocardial metabolism remained aerobic regionally and globally. Thus, the results suggest that blood pressure was easy to control and that there were no adverse effects on atrioventricular conduction, cardiac performance, regional and global myocardial oxygen utilization, or lactate extraction.

Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 ± 15 before and 739 ± 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine. However, the fact that levodopa and carbidopa were equally effective despite concurrent administration of domperidone favors an involvement of the central nervous system as the most likely mechanism of reduced vasoconstriction.

Coronary vasoconstrictor response to cold pressor test in variant angina: Lack of relation to intracoronary thromboxane concentrations

To test the hypothesis that intracoronary concentrations of thromboxane (Tx)A 2 could influence the response to cold pressor test (CPT) in variant angina, great cardiac vein blood flow (by thermodilution) and the concentration of TxB 2 (the stable metabolite of TxA 2) in the great cardiac vein and aorta were measured under control conditions and during CPT in 14 patients with angina at rest associated with transient ST-segment elevation in the anterior leads. In seven patients pretreated with aspirin (intravenous administration of 3.6 mg/kg lysine salt of acetylsalicylic acid, corresponding to 2 mg/kg aspirin), TxB 2 baseline concentrations were lower in both the great cardiac vein (47 ± 19 vs 176 ± 88 pg/ml; p < 0.005) and the aorta (45 ± 16 vs 109 ± 56 pg/ml, p < 0.02) than in seven patients who were not taking cyclooxygenase inhibitors. In the two groups, great cardiac vein flow and anterior region coronary resistance were similar under control conditions. During CPT anterior region coronary resistance increased in patients pretreated with aspirin (from 1.97 ± 0.99 to 2.22 ± 1.11 mm Hg/ml/min; p < 0.02) and in patients without aspirin pretreatment (from 1.94 ± 0.43 to 2.06 ± 0.34 mm Hg/ml/min; p < 0.05), and the difference between the two groups was not statistically significant. Therefore the vasoconstrictor response of coronary vessels to CPT in variant angina is not influenced by the intracoronary TxB 2 concentrations and is not modified by aspirin pretreatment.

Effect of nicardipine on determinants of myocardial ischemia occurring during acute coronary occlusion produced by percutaneous transluminal coronary angioplasty

In 10 patients undergoing percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery (LAD), the clinical, electrocardiographic and hemodynamic effects of acute intravenous calcium channel antagonism with nicardipine (2 mg over 1 minute, followed by a constant infusion of 25 to 50 μg/min) were assessed during temporary LAD occlusion. Onset of myocardial ischemia during coronary occlusion was prevented or delayed after administration of nicardipine in 7 of the 10 patients. During infusion of nicardipine and during LAD occlusion, residual great cardiac vein blood flow increased in 9 of 10 patients compared with residual flow during occlusion before nicardipine (10%, p < 0.05). Nicardipine also decreased mean aortic pressure, but was associated with a reflex-mediated increase in heart rate. Overall, the double product, an index of global myocardial oxygen demand, decreased 7% (p < 0.05). Thus, nicardipine usually diminished ischemia induced by acute transient coronary occlusion by increasing collateral flow while oxygen demand decreased.

Myocardial ischemia during intravenous prostacyclin administration: Hemodynamic findings and precautionary measures

This study reports coronary and systemic hemodynamics, and metabolic responses to atrial pacing, prostacyclin (PGI 2), and lioprost, its stable analogue, in 16 patients with severe coronary obstruction as well as predominant narrowing in the left anterior descending artery. PGI 2 caused ischemia in six patients with low anginal threshold during pacing. In three of them ischemia was also precipitated by iloprost. Drugs were infused at therapeutic doses and were discontinued when pain occurred. Angina disappeared promptly (≤ 3 minutes) and spontaneously after the infusion of PGI 2, whereas after the analogue it was long lasting (≥ 5 minutes) and was relieved by 125 mg intravenous aminophylline, an antagonist of dipyridamole-induced coronary dilation. Ischemia was associated with a drug-induced decrease in arterial blood pressure and reflex tachycardia, and occurred despite increased great cardiac vein (GCV) blood flow and decreased resistance, which is consistent with either a failure of regional flow to increase proportionally to the metabolic demand or a subendocardial-subepicardial steal. However, the following findings favor the latter hypothesis: (1) heart rate and rate-pressure product at the onset of pain were lower with drugs than with pacing, and (2) GCV blood flow, measured at a comparable heart rate, was less with pacing than with drugs. In conclusion, PGI 2 and analogues may induce ischemia in patients with advanced coronary artery disease. The mechanism appears to be related to a dipyridamole-like maldistribution of flow. Counteraction of ischemia can be achieved by aminophylline.

Alterations in regional myocardial blood flow after nitroprusside and nitroglycerin in patients with and without significant coronary artery disease

To evaluate vasodilator-induced redistribution of regional myocardial blood flow, intravenous sodium nitroprusside and nitroglycerin were administered in doses producing matched reductions (15%) in mean arterial pressure at constant heart rate. Anterior left ventricular great cardiac vein blood flow (thermodilution) was measured in 14 patients without angiographic anterior collateral supply. Global coronary sinus blood flow remained constant with both nitroprusside and nitroglycerin administration, despite significant reductions in mean arterial pressure. However, nitroglycerin reduced great vein flow by 25 ± 17% and nitroprusside by 10 ± 16% (p < 0.01). Subgroup analysis indicated that the nitroglycerin-nitroprusside regional blood flow differences were more pronounced in patients without significant left anterior descending coronary artery narrowing. Neither vasodilator produced significant differences in arterial-coronary sinus oxygen or lactate contents, calculated myocardial oxygen consumption, left ventricular dP/dt, or electrocardiographic or clinical signs of myocardial ischemia. Despite qualitatively similar hemodynamic effects, comparisons of vasodilator-induced relative reductions in normally supplied anterior left ventricular regional coronary blood flow suggest a mechanism of the reported beneficial effects of nitoglycerin on potentially ischemic myocardial regions.

Dose-related effects of intracoronary nitroglycerin on coronary hyperemia in patients with coronary artery disease

Although intracoronary nitroglycerin (NTG) is frequently required during percutaneous transluminal coronary angioplasty or thrombolysis, the dose-related hemodynamic effects and the extent to which intracoronary NTG-induced coronary hyperemia is limited in patients with coronary artery disease have not been defined. Therefore, we studied 19 patients with coronary artery disease (nine with no or minimal luminal narrowing of the left anterior descending coronary artery [group 1] and 10 with significant left anterior descending coronary stenosis [group 2]); mean arterial pressure and thermodilution coronary sinus and great cardiac vein blood flow were measured during bolus administrations of 50, 200, and 300 μg of intracoronary NTG. During the NTG-induced hyperemia, mean arterial pressure decreased 0%, 4% (bothp =NS), and 6% (p < 0.05) after 50, 200, and 300 μg doses, respectively. Heart rate did not change. Global coronary hyperemia was greatest for 200 μg with coronary blood flow increasing (74 ± 32% in group 1 and 53 ± 25% for group 2) but was significantly different from 50 μg only in group 2 patients. Moreover, the regional coronary blood flow responses were attenuated in group 2 compared to group 1 for 50 μg, 18 ± 13% vs 38 ± 18%, and for 200 μg, 35 ± 15% vs 72 ± 34% (bothp < 0.05), with the reduction of regional coronary resistance in group 2 attenuated for all three doses of intracoronary NTG. The 300 μg dose did not provide further augmentation of either global or regional coronary blood flow or greater reduction in coronary resistance. We conclude that intracoronary NTG-induced hyperemia is, in part, dose related and attenuated in patients with severe coronary artery disease. These data reemphasize the reduction in coronary vasodilatory reserve in regions supplied by coronary arteries with severe stenoses. Moreover, during interventions requiring intracoronary NTG, doses above 200 μg do not appear to further augment coronary blood flow, probably because of NTG-induced systemic hemodynamic effects and coronary autoregulation.

A microcomputer system for analysis of coronary artery calibre and blood flow.

Measurement of myocardial blood flow and assessment of coronary calibre in man has important clinical and research value. An inexpensive microcomputer system has been developed to facilitate analysis of each of these. Coronary sinus and great cardiac vein blood flow are measured using the thermodilution technique. The output of the temperature measurement circuitry is digitized and used to calculate blood flows. For coronary artery calibre measurement, the outline of an arterial segment recorded during coronary arteriography is digitized manually. The microcomputer system provides a graphic display of the digitized artery and calculates diameters throughout its length. Excellent correlations were observed between computer and manual methods for both systems.

Effects of pulsed external augmentation of diastolic pressure on coronary and systemic hemodynamics in patients with coronary artery disease

The purpose of this study was to define the effects of pulsed external diastolic pressure augmentation on coronary and systemic hemodynamics in 14 men with coronary artery disease and normal left ventricular function. Coronary sinus and great vein blood flow (thermodilution) and systemic hemodynamics were measured before, during, and after timed lower extremity compression, augmenting peak diastolic pressure to within 5 mm Hg of systolic pressure. Systolic and diastolic pressure-time indices were calculated from the high-fidelity micromanometer left ventricular-aortic recordings. External counterpulsation increased mean arterial pressure (108 ± 11 [1 SD] to 114 ± 12 mm Hg, p < 0.01) and the diastolic pressure-time index (440 ± 51 to 498 ± 82 units, p < 0.01), with no change in the systolic pressure-time index, absolute coronary sinus, or great cardiac vein blood flow. External diastolic pressure augmentation did not affect heart rate, right heart hemodynamics, cardiac output, or calculated myocardial oxygen consumption. An unanticipated finding was a ≥ 10% reduction in peak systolic pressure during external diastolic pressure augmentation in 8 of 14 patients. Despite minimal changes in absolute myocardial blood flow and oxygen consumption, the increase in the diastolic pressure-time/systolic pressure-time index ratio suggests that subendocardial perfusion may be favorably influenced by diastolic pressure augmentation and may explain the previously reported clinical benefits of external counterpulsation in some patients with ischemic heart disease.