Great Cardiac Venous Flow Research Articles

Differential coronary hemodynamics and left ventricular contractility in patients with syndrome X

The relationship between coronary hemodynamics and left ventricular contractility was studied in 20 patients with syndrome X. Among them, 10 patients with a resting left ventricular ejection fraction (LVEF, by radionuclide method) equal to or greater than the mean value of the whole group (58%) were defined as having relative increased left ventricular contractility (group H), and another 10 patients with relatively normal contractility (50%≤LVEF<58%) were in group N. Eight subjects with normal contractility, exercise test and coronary angiograms served as the control (group C). Baseline great cardiac venous flow (GCVF) was higher in group N than in group H ( P<0.05) and C ( P<0.05), but similar between group H and C. After dipyridamole infusion (0.56 mg/kg, i.v., for 4 min), maximum GCVF was less in group H than in group N ( P<0.001) and C ( P<0.001), but similar between group N and C. As compared to group C (3.09±0.35), coronary flow reserve was reduced in both group H (2.34±0.55, P=0.004) and N (2.40±0.36, P=0.001). In all syndrome X patients, resting LVEF was negatively correlated to baseline GCVF ( P=0.026) and tended to be positively correlated to baseline coronary vascular resistance ( P=0.057). Thus, coronary hemodynamics was altered with left ventricular contractility in syndrome X patients. In these patients, coronary flow reserve was similarly reduced with different underlying mechanisms. The limited increase of GCVF after dipyridamole infusion suggests impaired coronary microvascular dilation capacity in patients with relatively increased left ventricular contractility and the increase of baseline GCVF in those with normal contractility is more likely due to an altered basal myocardial metabolism.

Differential coronary microvascular function in patients with left ventricular dysfunction of unknown cause — implication for possible mechanism of myocardial ischemia in early stage of cardiomyopathy

To evaluate whether or not coronary microvascular dysfunction is associated with exercise-induced myocardial ischemia in left ventricular dysfunction of unknown cause, both the treadmill exercise test (TET) and coronary hemodynamics were studied in 20 patients with impaired left ventricular ejection fraction (<50% by radionuclide ventriculogram), normal cardiac size, normal coronary angiogram and no evidence of clinical heart failure. Ten subjects with atypical chest pain were studied as the control. Coronary hemodynamics were studied both at baseline and after dipyridamole infusion (0.56mg/kg, i.v. for 4′). There was no difference in age, gender, blood pressure, baseline great cardiac venous flow (GCVF) and coronary vascular resistance between ten patients with a positive TET and the other ten with a negative TET. At baseline, coronary sinus oxygen concentration was increased and myocardial oxygen consumption reduced in patients with a positive TET compared with those with negative a TET. After dipyridamole infusion, maximum GCVF (102±47 vs. 144±31 ml/min, P=0.027) and coronary flow reserve (2.31±0.49 vs. 3.00±0.61, P=0.012) were significantly reduced and minimum coronary vascular resistance was higher (1.00±0.42 vs. 0.63±0.12 mmHg/ml/min, P=0.016) in patients with a positive TET than in those with a negative TET. At follow-up, 40% of patients with a positive TET and 10% of those with a negative TET developed clinical heart failure with a dilated left ventricle during a period of 45 months. Thus, coronary microvascular function is heterogeneous in patients with left ventricular dysfunction of unknown cause. In some of them, coronary microvascular dysfunction could be related to the presence of exercise-induced myocardial ischemia, suggesting that similar pathophysiology underlies the early stage of dilated cardiomyopathy and syndrome X.

Early Alteration of Coronary Hemodynamics in Late Restenosis after Coronary Angioplasty

It is not known whether changes in coronary hemodynamics may antedate the development of restenosis after percutaneous coronary transluminal angioplasty (PTCA). The purpose of this study was to evaluate the early change in coronary microvascular function in patients with late restenosis after PTCA. Coronary hemodynamics were studied in series before, immediately after, 2 weeks and 3 months after successful PTCA in 12 male patients with a single lesion of the left anterior descending coronary artery. In each patient, great cardiac venous flow (GCVF) and oxygen content were measured both at baseline and during hyperemia induced by adenosine infusion. The sequential changes of coronary hemodynamics were compared between patients with and without restenosis at 3 months after PTCA. Basic characteristics did not differ between the patients with (n = 6) and those without restenosis (n = 6). Luminal diameter stenosis (in percentage) was also similar between the two groups both before (79.2 +/- 18.4% vs 83.0 +/- 9.6%, p = NS) and up to 2 weeks after PTCA (25.8 +/- 10.9% vs 28.5 +/- 7.9%, p = NS). In patients without restenosis, basal and hyperemic GCVF was unchanged up to 2 weeks after PTCA. There was a significant increase in CFR 3 months after PTCA. In patients with restenosis, basal GCVF was significantly increased and hyperemic GCVF was unchanged immediately after PTCA. However, 2 weeks after PTCA, basal GCVF was decreased while luminal diameter was still preserved. In comparison with those without restenosis, patients with restenosis had significantly lower CFR before (1.98 +/- 0.42 vs 2.69 +/- 0.46, p = 0.019), immediately after (1.47 +/- 0.27 vs 2.24 +/- 0.47, p = 0.006) and 3 months after PTCA (1.51 +/- 0.32 vs 3.40 +/- 0.54, p = 0.001). In patients without restenosis, the recovery of coronary microvascular function was delayed up to 3 months after PTCA. In patients with late restenosis, basal coronary microvascular tone was altered within 2 weeks after PTCA suggesting early deterioration of coronary microvascular function before the development of angiographic restenosis.

Temporal increase in resting coronary blood flow causes an impairment of coronary flow reserve after coronary angioplasty

Impaired coronary flow reserve immediately after coronary angioplasty may be attributed to an increase in resting coronary blood flow. To test this hypothesis we measured great cardiac venous flow (GCVF) at rest and during rapid atrial pacing before and immediately after angioplasty in 22 patients with significant narrowing of the left anterior descending artery and 12 patients (control group) with minimal narrowing. A follow-up (6 months) study was also done in seven patients. Immediately after angioplasty the coronary flow reserve (peak GCVF during pacing/resting GCVF) was not fully restored (1.5 ± 0.36 before angioplasty, 1.76 ± 0.42 after angioplasty, and 2.13 ± 0.33 in the control group). Resting coronary vascular resistance (2.4 ± 0.9 mm Hg/ml/min) was significantly decreased after angioplasty (2.0 ± 0.8 mm Hg/ml/min), whereas coronary vascular resistance during rapid pacing was fully restored to normal. Resting hyperemia was restored 6 months later, whereas coronary vascular resistance during pacing was unaltered. In five patients, however, slight ischemic ST-T changes were observed during rapid pacing, even after successful angioplasty associated with a decrease in the lactate extraction ratio. These results indicate that the impaired coronary flow reserve immediately after angioplasty may be attributed mainly to the temporal but significant increase in resting coronary flow, although impaired coronary vascular response to augmented myocardial oxygen demand may also be partially involved.

Effect of blood filling in intramyocardial vessels on coronary arterial inflow

The influence of the filling condition of the unstressed volume (UV) of intramyocardial vessels on the diastolic coronary arterial pressure-flow relationship was analyzed. UV is defined as the blood volume at zero transmural pressure. In seven anesthetized, paced dogs with induced heart block, coronary artery inflow was occluded so that blood in the UV was displaced into the coronary vein by myocardial contraction. After pacing was turned off, coronary perfusion pressure was increased stepwise to seven target pressures (20-90 mmHg). After reperfusion, left anterior descending coronary arterial (LAD) flow reached an initial quasi-steady level, but great cardiac venous (GCV) flow was absent (UV-unfilled phase). With reappearance of the GCV flow (UV-filled phase), LAD flow decreased to a final steady level. Pressure-flow relationships during both phases were linear (r = 0.97-0.99). The inverse of the slope of the pressure-flow relationship during the UV-filled phase, 0.69 +/- 0.08 mmHg.min.ml-1, was significantly higher than that during the UV-unfilled phase, 0.55 +/- 0.06 mmHg.min.ml-1 (P less than 0.01), although the zero-flow pressure intercepts were similar (18.9 +/- 1.8 mmHg for UV filled vs. 19.9 +/- 2.2 for UV unfilled). These results indicate that diastolic coronary arterial inflow is impeded by a blood volume within intramyocardial vessels that exceeds the UV.

Coronary flow reserve and diastolic dysfunction in hypertrophic cardiomyopathy

We studied 14 patients with hypertrophic cardiomyopathy during and after atrial pacing by simultaneous registration of left ventricular high fidelity pressure measurements and M-mode echocardiography together with great cardiac vein flow measured by thermodilution. Heart rate rose from 75 ± 18 to 142 ± 14 beats/minute with an increase of 93 ± 30 to 127 ± 46 milliliters/minute of great cardiac vein flow (increase 3f flow/beat: 0.8 versus 1.5 milliliters/beat in normal individuals; P < 0.05). In addition, diastolic hemodynamic parameters (such as left ventricular end-diastolic pressure, T 1 (time constant of relaxation) (of first 40 milliseconds) and T 2 (of second 40 milliseconds) and LVdP dt- ) changed from, respectively, 27.4 ± 7.1 to 24.0 ± 10.3 mm Hg; (NS), 67.3 ± 16.1 to 65.7 ± 22.2 liters/second; (NS) 68.6 ± 36.9 to 52.9 ± 19.4 ( P < 0.05), and 1592 ± 75 to 1302 ± 48 mm Hg/sec; P < 0.05. Left ventricular end-diastolic dimensions decreased whereas end-diastolic wall thickness increased from, respectively, 37 ± 3 to 34 ± 4 millimeters; ( P < 0.05) and 14 ± 2 to 17 ± 1 millimeters ( P < 0.05). Eleven of the 14 patients experienced angina pectoris concomitant with ST-T depression of 1 millimeter or more on the electro-cardiogram. No correlations were found between great cardiac venous flow and hemodynamically or ultrasonically derived diastolic parameters of left ventricular function.

Regional cardioprotection by subselective intracoronary nifedipine is not due to enhanced collateral flow during coronary angioplasty

Twelve patients with proximal stenosis of the left anterior descending artery, normal myocardial wall motion but without angiographically demonstrable collateral circulation, were studied during transluminal occlusion. Prior to the first transluminal occlusion before crossing the lesion with the balloon, patients were randomly given 0.2 mg nifedipine or its solvent in the left mainstem. The same dose was repeated via the balloon catheter, positioned across the lesion, immediately prior to the second transluminal occlusion. In all patients great cardiac venous flow and ST-elevation were monitored during and after each transluminal occlusion. The lactate extraction ratio A-GCV A (A = arterial, GCV = great cardiac vein) was determined prior to the angioplasty procedure, 10–15 seconds after each transluminal occlusion and 10 minutes after the third transluminal occlusion. Great cardiac venous flow rose significantly to an average of 160% of basal flow when nifedipine was administered into the mainstem before the angioplasty procedure while its solvent had no effect. During each transluminal occlusion, great cardiac venous flow diminished on average by 30% in those who received nifedipine and by 28% in those who received only its solvent. This difference was statistically not significant. After angioplasty great cardiac venous flow was slightly, but not significantly, increased in both groups with respect to basal flow (104% resp. 120% of control). Patients who received nifedipine in the post-stenotic area just before the second transluminal occlusion, had significantly lower lactate production, measured immediately after the transluminal occlusion compared with the patients who received only its solvent ( P<0.01). The ST-elevation during the second transluminal occlusion was significantly lower in the nifedipine group (0.1 mm in nifedipine group versus 1.4 mm in solvent group; P<0.05, unpaired t-test). Nifedipine given intracoronary in the post-stenotic area just before coronary angioplasty reduces lactate release and electrocardiographic signs of myocardial ischemic injury. This regional cardioprotective effect seems not due to an enhanced collateral flow, but to a regional cardioplegic effect, which precedes the ischemic event.

Regional Coronary Hemodynamics during Isoflurane???Nitrous Oxide Anesthesia in Patients with Ischemic Heart Disease

The effects of 1.5 MAC isoflurane-nitrous oxide anesthesia on central hemodynamics, regional coronary blood flow, myocardial oxygenation, and lactate balance were investigated in 13 patients with coronary artery disease. Mean arterial pressure was reduced 45% mainly because of systemic vasodilation. Great cardiac venous flow (GCVF) decreased, whereas total coronary sinus blood flow (CSF) was unchanged. Total coronary resistance and resistance in the area drained by the GCVF decreased as did myocardial oxygen extraction, demonstrating coronary vasodilation. The GCVF/CSF ratio did not decrease despite the reduction in resistance to left ventricular ejection. Seven patients had ECG and metabolic indications of myocardial ischemia (lactate extraction reduced from 22 +/- 5% to 7 +/- 3%, P less than 0.02 for the group). Changes in GCVF and oxygen consumption in the corresponding area correlated closely (r = 0.943). However, the regression line was shifted to the left and three patients, who became ischemic, had an increase in GCVF despite unchanged or decreased myocardial oxygen demand. It is concluded that isoflurane may cause coronary blood flow redistribution with regional myocardial ischemia in patients with coronary artery disease.

Validity of contrast hyperemia for clinical assessment of coronary flow reserve: the optimal dose of contrast medium and reproducibility of the technique.

The dose-response relation of contrast medium-induced hyperemic response in coronary blood flow (contrast hyperemia) was investigated to determine the optimal dose of contrast medium (CM, Urografin-76) for the assessment of coronary flow reserve in man. The great cardiac venous flow (GCVF) was determined with the continuous thermodilution method during the contrast hyperemia induced by the intracoronary injection of CM of three different doses, ie, 2, 4, and 6 ml/60 kg of body weight, into left coronary artery. Submaximal coronary vasodilation could be obtained by intracoronary injection of 4 ml of CM with minimal changes in systemic hemodynamics. The contrast hyperemia with this dose of CM was reproducible and also closely correlated with that obtained during pacing-induced angina. Thus, we conclude that the contrast hyperemic technique with intracoronary injection of 4 ml of Urografin-76 could be a reliable method to assess the coronary flow reserve.