Humans have pre-formed collateral vessels that enlarge with ischemia. In addition, new vessels can be formed within ischemic zones from pre-formed endocardial arcades of vessels providing rich collateral flow. Collateral flow under resting conditions (if >25% of normal) is enough to maintain myocardial viability, but may be insufficient to prevent myocardial ischemia under stress. Coronary angiography is a poor tool for collateral flow assessment. Myocardial contrast echocardiography is arguably the gold standard for experimental and clinical measurement of collateral flow. This review describes several experimental and clinical studies that highlight the importance of the collateral circulation in coronary artery disease.
Collateral Circulation ; Coronary Angiography ; Coronary Artery Disease ; Echocardiography* ; Humans ; Ischemia ; Myocardial Ischemia

OBJECTIVETo investigate the effects of nitroglycerine (NTG) on myocardial oxygen metabolism and regional cardiac function in canine hearts with a stable systemic hemodynamics in situ.

METHODSEight anesthetized open-chest dogs with flow-limited left anterior descending branch of the coronary artery or left circumflex artery (LCx) stenosis were studied. The percentage of ventricular wall thickening (%WT) was measured with quantitative two-dimensional echocardiography (2DE), myocardial blood flow (MBF) with radiolabeled microspheres and tissue oxygen pressure (tPO(2).) with oxygen-dependent quenching of phosphorescence. 2DE was performed and radiolabeled microspheres and Pd-porphyrin injected in the dogs at rest during intracoronary infusion of 0.3-0.6 mg x kg(-1) x min(-1) of NTG. Myocardial oxygen consumption (MVO(2), ml x min(-1) x 100 g(-1)) was calculated as the multiplication product between the arterio-venous oxygen content difference and MBF, and myocardial O(2) delivery as the product between arterial oxygen content and MBF.

RESULTSAs compared with the baseline, NTG increased %WT and MBF significantly in both normal and ischemic beds (P<0.05). There was a significant increase in MVO(2) during NTG infusion in the ischemic bed (P<0.05) in comparison with that measured at rest. NTG, however, significantly increased the ability of myocardial O(2) delivery in both normal and ischemic beds (P<0.05), therefore tPO(2) was still higher in the ischemic bed during NTG infusion than that at rest (P<0.05). The percentage increment in tPO(2) was significantly greater in the ischemic bed than percentage MBF increment.

CONCLUSIONSNTG enhances myocardial oxygen concentration in normal and ischemic myocardium and may increase oxygen release to the ischemic myocardium in vivo. NTG may have a positive inotropic effect on regional cardiac function. In addition to direct effect on vascular tone, NTG plays important roles in the cardiovascular system by modulating myocardial oxygen metabolism and contractile function.

Animals ; Dogs ; Echocardiography ; Hemodynamics ; Myocardium ; metabolism ; Nitroglycerin ; pharmacology ; Oxygen Consumption ; drug effects

OBJECTIVETo evaluate the direct effects of dobutamine as compared to adenosine on the coronary microcirculation in both normal and stenotic segments using myocardial contrast echocardiography (MCE).

METHODSLeft anterior descending (LAD) coronary artery stenosis, which was not flow limiting at rest, was established in 9 dogs. At the baseline and during intracoronary infusion of dobutamine (2 mg.kg(-1).min(-1)) and adenosine (5 mg.kg(-1).min(-1)), the radiolabeled microsphere (RM)-derived myocardial blood flow (MBF) were determined, and the double product (DP) and myocardial vascular resistance (MVR) were calculated. MCE was performed to determine the myocardial blood volume (MBV, represented by A) and microbubble velocity (beta).

RESULTSAs compared to the baseline level, the MBF increased and MVR decreased significantly in both the normal and abnormal beds during infusion of both drugs (P<0.05). In the normal bed, adenosine had no effect on MBV, the decrease in MVR was the result of decreased arteriolar (plus venular) resistance, and the increase in MBF was predominately due to the increase in b (deltabeta/ deltaA=13.6). Dobutamine caused a 28% increase in MBV, responsible for 32% of the decrease in the total MVR, but the increase in MBF arose mainly from the increase in b (deltabeta/deltaA=5.9). In the abnormal bed, both the drugs caused a similar increase in MBF entirely by increasing b, and 14% and 15% of the increases in capillary resistance were associated with the capillary derecruitment during administration of dobutamine and adenosine, respectively.

CONCLUSIONThe direct effects of intracoronary dobutamine infusion on the coronary microcirculation are similar to that of adenosine, and the increase in MBF occurs mostly as the result of increased myocardial blood velocity.

Adenosine ; pharmacology ; Adrenergic beta-Agonists ; pharmacology ; Animals ; Blood Flow Velocity ; drug effects ; Coronary Circulation ; drug effects ; Coronary Stenosis ; diagnostic imaging ; Coronary Vessels ; diagnostic imaging ; Dobutamine ; pharmacology ; Dogs ; Echocardiography ; methods ; Microcirculation ; drug effects ; Vasodilator Agents ; pharmacology