Collateral Blood Flow In Patients Research Articles

Improvement of Exercise Capacity by Sarpogrelate as a Result of Increased Collateral Blood Flow in Patients With Effort Angina

Improvement of Exercise Capacity by Sarpogrelate as a Result of Increased Collateral Blood Flow in Patients With Effort Angina

Improvement of exercise capacity by sarpogrelate as a result of increased collateral blood flow in patients with effort angina

Improvement of exercise capacity by sarpogrelate as a result of increased collateral blood flow in patients with effort angina

Comparison of bronchopulmonary collaterals and collateral blood flow in patients with chronic thromboembolic and primary pulmonary hypertension.

OBJECTIVE: To compare the visualisation of bronchopulmonary collaterals and bronchopulmonary collateral blood flow in patients with chronic thromboembolic pulmonary hypertension 2nd primary pulmonary hypertension. SETTING: Referral centre for cardiology at...

Computer modeling of cerebral blood flow following internal carotid artery occlusion.

It is difficult to predict the adequacy of the collateral blood flow in patients who undergo internal carotid artery occlusion. In order to address this difficulty, the authors have created a computer model of the cerebral circulation. This model features individualized simulations of the Circle of Willis and its afferent and efferent branches which can predict changes in flow that will occur during internal carotid artery occlusion. Analysis of the flow predictions suggests that in patients with a symmetric Circle of Willis the anterior communicating artery is the major conduit of collateral blood supply. In patients with a small anterior communicating artery, the posterior communicating arteries become more important as sources of collateral flow, but they cannot supply as much flow as in the case of a normal anterior communicating artery. Sensitivity studies show that changes in the dimensions of each artery affect the flow throughout the system, such that the arteries in the cerebral circulation must be analyzed as a network rather than as isolated elements. This computer model of the cerebral circulation may help clinicians predict the adequacy of collateral blood supply in patients who undergo internal carotid artery occlusion.

Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis

Background: Changes in intra-abdominal pressure (IAP) have significant circulatory effects. However, whether this may influence the gastroesophageal collateral blood flow in patients with cirrhosis has not been studied. Methods: In 14 portal hypertensive cirrhotics, serial hemodynamic measurements were obtained in baseline conditions 30 minutes after the mechanical increase of IAP by 10 mm Hg and 30 minutes after returning IAP to baseline levels. Results: Increasing IAP caused similar increases in free and wedged hepatic venous pressures (+10.3 mm Hg and +11.0 mm Hg, respectively; P < 0.005), without changing the hepatic venous pressure gradient (HVPG). However, there were significant decreases in cardiac output (−18%; P < 0.005) and hepatic blood flow (−20%; P < 0.05), whereas azygos blood flow, an index of gastroesophageal collateral blood flow, increased markedly (+23%; P < 0.005). The opposite occurred after releasing the high IAP. Conclusion: In portal hypertensive cirrhotics, acute changes in IAP did not change HVPG but markedly modified splanchnic and systemic hemodynamics. Brief elevations of IAP may have deletereous effects, as shown by the increase in azygos blood flow and the decrease in cardiac output and hepatic blood flow, whereas reduction of a high IAP causes the opposite changes and may be beneficial.

Functional significance of collateral blood flow in patients with recent acute myocardial infarction. A study using myocardial contrast echocardiography.

We hypothesized that myocardial contrast echocardiography (MCE) can be used to both measure collateral blood flow as well as assess the functional significance of collaterals in patients with acute myocardial infarction (AMI). MCE was performed in 33 patients with recent AMI (12 +/- 7 days) and an occluded infarct-related artery (IRA), both before and after attempted percutaneous transluminal coronary angioplasty (PTCA). The size of the occluded bed was defined in patients with successful PTCA by injecting contrast directly into the opened IRA and expressed as a percent of the myocardium in the short-axis view. The percent of the perfusion bed supplied by collaterals before PTCA was determined. Transit rates of the microbubbles within the collateralized regions were also measured and were expressed as a percent of the transit rates in the normal adjacent beds. Regional function within the occluded bed was assessed using echocardiography and was graded as 1 (normal) to 5 (dyskinetic). Collaterals were graded on coronary angiography as 0 (none) to 3 (abundant). The perfusion bed size was larger for the left anterior descending (LAD) than for the right (RCA) and left circumflex (LCx) coronary arteries (37 +/- 6% versus 27 +/- 12% of the myocardium, p = 0.02). The percent of the occluded bed supplied by collateral flow was greater for RCA and LCx compared with the LAD (87 +/- 30% versus 72 +/- 22%, p less than 0.01). There was poor correlation between MCE-defined percent of occluded bed supplied by collaterals and angiographic collateral grade (r = 0.13). Regions supplied by collaterals were less likely to show confluent hypoperfused zones after reperfusion compared with those not supplied by collaterals. Similarly, the percent of myocardium not perfused by either anterograde or collateral flow correlated well (r = 0.67, p less than 0.01) with peak creatine kinase levels and was more likely to be associated with Q waves. Finally, although there was poor correlation between angiographic collaterals and regional function (r = 0.20), there was a significant negative correlation between MCE-defined spatial extent of collateral flow and regional function (r = -0.57, p less than 0.01). MCE can be used to measure collateral flow in patients with recent AMI and to assess the functional significance of collaterals in these patients. This technique may be ideally suited for the assessment of collateral perfusion in patients undergoing cardiac catheterization.

The Effects of Ethanol Administration on Portal Pressure and Gastroesophageal Collateral Blood Flow in Patients With Alcoholic Cirrhosis

The pathogenesis of variceal hemorrhage is not well understood. Portal pressure and gastroesophageal collateral (azygous) blood flow are similar in patients with cirrhosis with or without a history of variceal bleeding. However, acute increases in these parameters in individual patients might predispose them to variceal rupture. Fifteen patients with alcoholic cirrhosis and portal hypertension were evaluated to test the hypothesis that ethanol intake acutely increases portal pressure or gastroesophageal blood flow and is a possible risk factor in variceal hemorrhage. A 10% solution of ethanol in 5% dextrose in water was infused intravenously at a rate sufficient to raise the blood-alcohol level to 100 mg/dl over 30 min. Eight patients received ethanol 5% dextrose in water; seven patients received a placebo (5% dextrose in water alone). Ethanol did not produce a significant change in wedged hepatic-vein pressure, free hepatic-vein pressure, azygous blood flow, mean arterial pressure or heart rate compared with the effects of 5% dextrose in water alone. Acute administration of ethanol does not increase portal pressure or gastroesophageal blood flow. It is unlikely that acute ethanol ingestion is a risk factor for variceal hemorrhage.

Portal hypertension: Serotonin and pathogenesis

It has been demonstrated that serotonin (5-hydroxytryptamine; 5HT) can decrease portal vascular resistance in animals and could be a possible mediator for intestinal vasodilatation. Moreover, isolated mesenteric vein from portal hypertensive rats has been shown to be hyper-responsive to 5HT. Hence 5HT may play a role in the pathophysiology of the hyperkinetic syndrome observed in patients with portal hypertension. This hypothesis that serotonin might increase splanchnic blood flow, and hence portal pressure, led us to propose that 5HT receptor antagonists might decrease portal hypertension. We observed that acute administration of ketanserin, an antagonist of serotonin at 5HT2 receptors, significantly decreased portal pressure and portal-systemic collateral blood flow in patients with cirrhosis, whereas hepatic blood flow was not modified. Arterial pressure slightly decreased, while cardiac output was not affected by ketanserin. These findings were also observed during continuous administration of ketanserin. More recently, it has been shown that ritanserin, a more specific 5HT2 receptor antagonist, significantly decreased portal pressure in cirrhotic patients. Finally, in rats with portal hypertension, ketanserin as well as ritanserin produced significant reductions in portal pressure but did not modify portal tributory blood flow. In these portal hypertensive animals, 5HT2 antagonists may act on hepatocollateral vascular resistance. These studies confirm current evidence in favor of a role for the actions of serotonin via 5HT2 receptors in portal hypertension and add a new group of substances for its treatment.

Combination of ketanserin and verapamil or propranolol in patients with alcoholic cirrhosis: search for an additive effect.

Drugs reported to reduce portal pressure through different mechanisms were combined in the hope of either additive portal hypotensive effects in "responders," or inducing a portal hypotensive effect in "nonresponders" to the initial drug. Seven patients with alcoholic cirrhosis received verapamil, 10 mg i.v., and, 60 min later, ketanserin, 5 mg i.v. Verapamil decreased heart rate and increased free hepatic venous pressure but had no effect on hepatic venous pressure gradient or azygos blood flow. When combined with verapamil, ketanserin significantly diminished wedged hepatic venous pressure and hepatic venous pressure gradient. Ten other patients with alcoholic cirrhosis received propranolol, 15 mg i.v., and 45 min later, ketanserin, 5 mg i.v. In all patients, heart rate, cardiac index and azygos blood flow significantly decreased after propranolol. After propranolol alone, however, wedged hepatic venous pressure decreased in only five patients, responders. In five other patients, defined as nonresponders, propranolol did not decrease this pressure. The addition of ketanserin to propranolol induced further significant reduction in wedged hepatic venous pressure, hepatic venous pressure gradient and azygos blood flow. Among the five nonresponders, three had a reduced wedged hepatic venous pressure after ketanserin was combined. We conclude that verapamil does not reduce portal pressure or collateral blood flow in patients with alcoholic cirrhosis. The splanchnic hemodynamic effects of propranolol and ketanserin appear to be independent and additive, without significant systemic alteration.

Semiquantitative evaluation of ophthalmic collateral flow in carotid artery occlusion: ultrasonic doppler study.

The reliability of quantitative evaluation by doppler ultrasound with regard to the ophthalmic collateral blood flow in patients with carotid artery occlusion was estimated. The ultrasonic doppler flow signals of the ophthalmic collateral flow of 54 carotid occlusions were classified into four types and three degrees--high, moderate, and low reversed flow patterns--and were compared with the angiographic findings of the collateral flow classified into three grades--good, poor, and none. With the exception of three cases, the ultrasonic doppler flow patterns of the collateral flow correlated well with the angiographic findings in 54 occluded carotid arteries.