Coronary Microvascular Vasodilatory Function: Related Clinical Features and Differences According to the Different Coronary Arteries and Types of Coronary Spasm

Background: In the clinical setting; the microvascular vasodilatory function test (MVFT) with a pressure wire has been used in ischaemia patients with non-obstructive coronary arteries (INOCA), including vasospastic angina (VSA) and microvascular angina (MVA). The exact factors that affect the microvascular vasodilatory function (MVF) in such patients are still unknown. We aimed to identify the factors, including clinical parameters and lesion characteristics, affecting the MVF in such patients. Methods: A total of 53 patients who underwent coronary angiography, spasm provocation tests (SPTs) and MVFTs were enrolled. In the MVFT, the coronary flow reserve (CFR) and index of microcirculatory resistance (IMR) were measured. Of the 53 patients, MVFT data in the left anterior descending coronary artery (LAD) were obtained from 49 patients, and the clinical parameters were checked in all of them. Based on the results of the SPT, coronary spasms were divided into focal spasm, diffuse spasm, and microvascular spasm (MVS). To assess the lesion characteristics influencing MVF, MVFT data were compared according to the types of coronary spasm and coronary vessels in 73 vessels of the 53 patients. Results: In 49 patients who underwent the MVFT in the LAD, the IMR was higher in active smokers (n = 7) than in former smokers (n = 15) and never smokers (n = 27, p < 0.01). In the 73 coronary arteries in this study, the type of coronary spasm did not correlate with the CFR or IMR, whereas a higher IMR were more frequently observed in cases of focal spasm than in cases of diffuse spasm (p = 0.03). In addition, the IMR was higher in the right coronary artery (RCA) than in the LAD (p = 0.02). Conclusion: These results indicate that the smoking status affected the MVF in patients with INOCA, suggesting the possibility of improvement in the MVF by smoking cessation in such patients. In addition, in the assessment of MVF, it may be important to take into account which coronary artery or types of coronary spasm are being evaluated.

The Effects of Cerebral Vasospasm on Cerebral Blood Flow and the Effects of Induced Hypertension: A Mathematical Modelling Study

Background: Induced hypertension has been used to promote cerebral blood flow under vasospastic conditions although there is no randomised clinical trial to support its use. We sought to mathematically model the effects of vasospasm on the cerebral blood flow and the effects of induced hypertension. Methods: The Anatomically Detailed Arterial Network (ADAN) model is employed as the anatomical substrate in which the cerebral blood flow is simulated as part of the simulation of the whole body arterial circulation. The pressure drop across the spastic vessel is modelled by inserting a specific constriction model within the corresponding vessel in the ADAN model. We altered the degree of vasospasm, the length of the vasospastic segment, the location of the vasospasm, the pressure (baseline mean arterial pressure [MAP] 90 mm Hg, hypertension MAP 120 mm Hg, hypotension), and the presence of collateral supply. Results: Larger decreases in cerebral flow were seen for diffuse spasm and more severe vasospasm. The presence of collateral supply could maintain cerebral blood flow, but only if the vasospasm did not occur distal to the collateral. Induced hypertension caused an increase in blood flow in all scenarios, but did not normalise blood flow even in the presence of moderate vasospasm (30%). Hypertension in the presence of a complete circle of Willis had a marginally greater effect on the blood flow, but did not normalise flow. Conclusion: Under vasospastic condition, cerebral blood flow varies considerably. Hypertension can raise the blood flow, but it is unable to restore cerebral blood flow to baseline.

Dysphagia after antireflux fundoplication: endoscopic, radiological and manometric evaluation

BACKGROUND: The transient dysphagia after fundoplication is common and most often disappears until six weeks postoperatively. AIM: Analyze a group of patients who presented late and persistent dysphagia postoperatively. METHODS: Forty-one patients after Nissen fundoplication, 14 male and 27 female, mean age 48 year, were evaluated based on medical history, esophagogastroduodenoscopy, contrast radiographic examination and esophageal manometry. The results were compared with another 19 asymptomatic individuals. RESULTS: Contrast radiographic examination of the esophagus revealed in six cases delayed emptying, characterizing that four patients had achalasia and two diffuse spasm of the esophagus. Esophageal manometry showed that maximal expiratory pressure of the lower sphincter ranged from 10 to 38 mmHg and mean respiratory pressure from 14 to 47 mmHg, values similar to controls. Residual pressure ranged from 5 to 31 mmHg, and 17 patients had the same values as the control group. CONCLUSION: The residual pressure of the lower sphincter was higher and statistically significant in patients with dysphagia compared with those operated without dysphagia. Future studies individualizing and categorizing each motility disorder, employing other techniques of manometry, and the analysis of the residual pressure may contribute to understand of persistent dysphagia in the postoperative fundoplication.

Cerebrovascular reactivity in patients with ruptured intracranial aneurysms

✓ The cerebral vasomotor reactivity to arterial hypotension and hypocapnia was studied in 34 patients between the 3rd and 13th day after rupture of an intracranial saccular aneurysm. Using the intra-arterial xenon-133 injection method, regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO2) were measured. The intraventricular pressure and cerebrospinal fluid (CSF) lactate and pH levels were determined. The degree of vasospasm was measured on angiograms taken immediately following the rCBF study. The patients were graded clinically according to the system of Hunt and Hess. Cerebral autoregulation was intact in patients in good clinical condition, but was impaired in patients in poor clinical condition. There was a close correlation between the degree of vasospasm and the degree of autoregulatory impairment, which varied from focal disturbances to global impairment. Intracranial hypertension and CSF lactic acidosis were commonly found in association with vasoparalysis. Cerebrovascular response to hyperventilation was generally preserved, although often reduced. During hyperventilation, the cerebral perfusion pressure became elevated, and increases in CMRO2 were often found, even in patients with severe diffuse spasm and cerebral ischemia. The clinical significance of the results in relation to the treatment of delayed cerebral ischemia and to the use of intraoperative induced hypotension is discussed.

Regional CBF, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms

✓ Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (CMRO2), intraventricular pressure, and lactate/pH levels in the cerebrospinal fluid (CSF) were measured in 38 patients with ruptured intracranial aneurysms between the 3rd and 13th day after subarachnoid hemorrhage (SAH). Angiography was performed following the rCBF study and the degree of vasospasm was measured on the angiograms. The patients were graded clinically according to the system of Hunt and Hess. Cerebral vasospasm significantly influenced rCBF: global reductions and focal changes (ischemia, hyperemia, and tissue peaks) were commonly associated with vasospasm. Patients with severe diffuse spasm always had global ischemia (21 ± 5 ml/100 gm/min), and cerebral infarctions were demonstrated subsequently, The CMRO2 was more reduced than rCBF, indicating an uncoupling between flow and metabolism. This relative luxury perfusion was associated with CSF lactic acidosis and intracranial hypertension. The arteriovenous difference of oxygen was equally reduced in all categories of patients, probably due to the primary insult of SAH. The CMRO2 decreased concomitantly with arterial caliber, indicating a secondary impairment of cerebral metabolism due to vasospasm.