[Coronary angiography and measurement of coronary circulation in coronary heart disease].
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Angiotensin is a potent coronary vasoconstrictor, but little is known of the effects of long-term activation of the renin-angiotensin system on coronary reserve in humans. The effects of exercise on coronary hemodynamics were determined in eight patients with mild essential uncomplicated hypertension, before and after treatment with furosemide (50 mg, to ensure activation of the renin-angiotensin system). Coronary sinus blood flow was measured by thermodilution technique, intra-arterial blood pressure was measured from the ascending aorta, and plasma renin activity was determined by radioimmunoassay. Oxygen supply and demand were derived (using coronary sinus blood flow multiplied by the arteriovenous oxygen difference to equal oxygen supply and heart rate multiplied by the mean systolic blood pressure to equal oxygen demand) both at rest and during isometric exercise (handgrip to 50 percent of maximal effort for three minutes). The study was a single-blind crossover (furosemide versus placebo) design. Furosemide produced a significant reduction in coronary sinus blood flow, associated with an increase in coronary vascular resistance. Changes in mean arterial pressure and heart rate were insignificant. Slight reductions in plasma volume and mean right atrial pressure were observed. During isometric exercise, the increase in oxygen supply for a given increment in oxygen demand was attenuated by furosemide. The contribution of the renin-angiotensin system to this effect was determined by the short-term administration of 25 mg of the angiotensin converting enzyme inhibitor captopril. Forty-five minutes after oral captopril, coronary reserve was restored to pretreatment values. In conclusion, furosemide modulates coronary reserve, and it is likely that this is because furosemide mediates activation of renin-angiotensin system, thus reducing the vasodilatory capacity of the coronary arteries.
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To evaluate effects of stellate ganglion block (SGB) on coronary circulation under coronary occlusion, the changes in cardiac function and tissue blood flow in the myocardial ischemic area after right and left SGB were observed in the dogs. Tissue blood flow in the myocardial ischemic area measured with laser doppler flowmeter showed no significant change after right or left SGB. In the right SGB group, heart rate, circumflex branch blood flow and rate pressure product decreased significantly (P < 0.01); end-diastolic pressure increased slightly (P < 0.05); myocardial oxygen extraction rate showed no significant change. On the other hand, in the left SGB group, heart rate, circumflex branch blood flow and rate pressure product showed no significant changes, while end-diastolic pressure and myocardial oxygen extraction rate increased significantly (P < 0.05). These data suggest that although right SGB might be useful to improve the oxygen demand-supply relation, left SGB does not improve the oxygen demand-supply relation and might increase the risk of myocardial ischemia.
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Recent studies have revealed that matrix metalloproteinases (MMPs) play an important role in cardiovascular remodeling by degrading the extracellular matrix. We investigated changes in the expression of MMPs due to percutaneous transluminal coronary angioplasty (PTCA). We studied 47 patients with ischemic heart disease who underwent elective PTCA on isolated stenotic lesion of left coronary arteries. Twelve patients received conventional balloon angioplasty, 14 percutaneous transluminal rotational atherectomy and 21 stent implantation. Blood samples were drawn from the coronary sinus immediately before and after, as well as 4 and 24 h, after PTCA. Plasma levels of MMP-1, MMP-2, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured by enzyme-linked immunosorbent assay. Plasma MMP-2 activity was determined with the digestion of a specific chromogenic peptide substrate. We could observe serial changes in plasma MMP-1 levels in the coronary circulation only in one patient, because MMP-1 levels were lower than the limit of detection in other patients. On the other hand, plasma MMP-2 levels in the coronary sinus were detectable in all subjects and increased significantly 4 and 24 h after PTCA. Plasma TIMP-1 levels also showed significant increases 4 and 24 h after PTCA, whereas TIMP-2 did not show significant changes. Plasma MMP-2/TIMP-2 ratio and MMP-2 activity in the coronary sinus showed significant increases 4 and 24 h after PTCA. A positive correlation was observed between MMP-2 levels in the coronary sinus 4 h after PTCA and late loss index 6 months after PTCA. MMP-2 levels in the coronary sinus blood were significantly higher in patients with late restenosis than in those without restenosis. PTCA induces increases in plasma MMP-2 levels and activity in the coronary circulation, which may contribute to vascular remodeling and late restenosis after PTCA.
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The coronary circulation holds a unique position among the different vascular beds because it perfuses the organ that generates the perfusion pressure for the entire circulation. Therefore the maintenance of an adequate perioperative coronary flow is one of the primary goals of good anesthetic management. This is especially important when coronary flow is already diminished such as is the case with arteriosclerotic disease. All anesthetics influence coronary flow to some extent. Some of them however also affect the normal physiologic responses of this system and may compromise coronary circulation and hence myocardial function. Therefore, knowledge of the coronary physiology and the effects of anesthetics on it is essential for every anesthetist dealing with patients with coronary artery disease. This article reviews the anatomy and physiology of the coronary circulatory system and resumes the present state of knowledge of the effects of the common used anesthetics on the coronary circulation.
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UNLABELLED: Coronary pressure flow (P/F) relationship has been investigated mainly from the viewpoint of coronary resistance. However, recent experimental evidence suggests that the zero flow pressure intercept (Pzf) provides important characteristics of coronary circulation. Although Pzf is likely to provide meaningful information about characteristics of coronary circulation, no data are available about Pzf in humans. The authors attempted to determine Pzf in humans by analyzing P/F relationship during long cardiac pause. This relationship, provoked by intracoronary adenosine triphosphate (ATP) infusion, was analyzed in 9 patients (8 men, 1 woman) with coronary heart disease (ages: fifty-six +/- six years). After the diagnostic cardiac catheterization, ATP, 0.6 mg/3 mL, was administrated by bolus intracoronary injection during measurements of coronary blood flow velocity. Coronary blood flow velocity in the left anterior descending artery was measured with a 0.018-inch Doppler angioplasty guide wire (FloWire, Cariometrics, Inc., Mountain View, Calif.). The dynamic P/F relationship was obtained by correlation of the instantaneous aortic pressure and flow velocity with each other at constant intervals. The least square linear regression analysis was applied to the P/F data to yield the extrapolated Pzf axis. Immediately after intracoronary injection of ATP, long pause (5320 +/- 1498 msec) appeared and coronary blood flow velocity decreased to 11 +/- 8 cm/sec. Pzf calculated with P/F relationship was 14 +/- 7 mmHg. CONCLUSIONS: Thus, the results clearly demonstrate that Pzf is higher than right atrial and left ventricular end-diastolic pressure in humans, indicating the complexity of the determinants of the Pzf.
The responses to hypocapnia and to hypercapnia of both the systemic and the coronary circulations have been studied in the dog during intermittent positive pressure ventilation under halothane anaesthesia. In the absence of significant variations of myocardial contractility, the reduction of cardiac output, because of hypocapnia, was determined by the increase of systemic vascular resistance, while the increase of cardiac output because of hypercapnia was determined by an increase of heart rate without change of stroke volume. The alterations of coronary blood flow (reduction following hypocapnia, augmentation following hypercapnia) were considerably larger than the changes of cardiac output and of myocardial oxygen consumption. Such disparity between oxygen supply and demand, together with the effect of pH and PCO2 on the oxyhaemoglobin dissociation curve led to a marked reduction of coronary sinus PO2 in response to hypocapnia and a marked increase of coronary sinus PO2 in response to hypercapnia. The data suggests that PCO2 (or respiratory alterations of pH) may have a direct effect on the regulation of coronary blood flow. The low coronary sinus PO2 observed at hypocapnia may suggest the risk of myocardial ischaemia.
Oxidized low-density lipoproteins are important in the progression of atherosclerosis. Autoantibodies against malondialdehyde-modified low-density lipoproteins have been reported to be predictive of the progression of atherosclerosis. This study sought to examine whether plasma levels of autoantibodies against oxidized low-density lipoprotein increase in the coronary circulation in patients with coronary spastic angina. The authors examined plasma antioxidized low-density lipoprotein antibody levels (activity unit values (AcU)/mL) simultaneously in the coronary sinus and the aortic root in 20 patients with coronary spastic angina, 23 patients with stable exertional angina, and 15 control subjects by measuring plasma levels of immunoglobulin G (IgG) autoantibodies against malondialdehyde-modified low-density lipoproteins by enzyme-linked immunosorbent assay. The plasma antioxidized low-density lipoprotein antibody levels (AcU/mL) in the coronary sinus increased in coronary spastic angina (38 +/- 16) compared with stable exertional angina (23 +/- 7) and control subjects (20 +/- 6) (p < or = 0.0001). The levels (AcU/mL) in the aortic root also increased in coronary spastic angina (33 +/- 12) compared with stable exertional angina (23 +/- 7) and control subjects (20 +/- 6) (p < 0.005). Furthermore, the coronary sinus-arterial differences of the levels (AcU/mL) were also higher in coronary spastic angina (5 +/- 9) than in stable exertional angina (0 +/- 6) and healthy subjects (-1 +/- 5) (p < 0.05). The generation of malondialdehyde-modified low-density lipoproteins is reported to be associated with atherothrombosis. These findings suggest that elevated levels of autoantibodies against malondialdehyde-modified oxidized low-density lipoproteins in coronary circulation are associated with the development of atherothrombosis from the progression of atherosclerosis rather than with the extent of coronary atherosclerosis in patients with coronary spastic angina.