Beware of delayed severe brain swelling after intracerebral haematoma in HELLP syndrome.

Haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome is a condition associated with increased risk of adverse outcomes during pregnancy and peripartum, including neurological complications. We report the third case in the world literature of delayed brain swelling following cerebral haemorrhage as a complication of HELLP syndrome. A 36-year-old woman in labour developed HELLP, which was complicated with intracerebral haematoma. This was evacuated, but motor impairment persisted after surgery and unfortunately the patient died unexpectedly during the 11th postoperative day. Computer tomographic brain scans documented diffuse cerebral swelling, which we think may have been caused by cerebral vasospasm. Cerebral vasospasm should always be considered when managing patients who suffered from stroke complicating HELLP syndrome. Close monitoring is advised even in later stages of recovery.

Major improvement of percutaneous cardiovascular procedure outcomes with radial artery catheterisation: results from the PREVAIL study.

OBJECTIVE: To obtain a "snapshot" view of access-specific percutaneous cardiovascular procedures outcomes in the real world. DESIGN: Multicentre, prospective study performed over a 30-day period. SETTING: Nine hospitals with invasive cardiology facilities, reflecting the contemporary state of healthcare. PATIENTS: Unselected consecutive sample of patients undergoing any percutaneous cardiovascular procedure requiring an arterial access. INTERVENTIONS: Percutaneous cardiovascular procedures by radial or femoral access MAIN OUTCOME MEASURES: The primary outcome was the combined incidence of in-hospital (a) major and minor haemorrhages; (b) peri-procedural stroke; and (c) entry-site vascular complications. The secondary outcome was the combined incidence of in-hospital death and myocardial infarction/reinfarction. For analysis purposes, outcomes were allocated to arterial access-determined study arms on an intention-to treat basis. Multivariable analysis adjusted using propensity score was performed to correct for selection bias related to arterial site. RESULTS: A total of 1052 patients were enrolled: 509 underwent radial access and 543 femoral access. In both groups, 40% underwent a coronary angioplasty. Relative to femoral access, radial access was associated with a lower incidence both of primary (4.2% vs 1.96%, p = 0.03, respectively) and secondary endpoints (3.1% vs 0.6%, p = 0.005, respectively). Multivariate analysis, adjusted for procedural and clinical confounders, confirmed that intention-to-access via the radial route was significantly and independently associated with a decreased risk both of primary (OR 0.37, 95% CI 0.16 to 0.84) and secondary endpoints (OR 0.14, 95% CI 0.03 to 0.62). CONCLUSIONS: Our study indicates strikingly better outcomes of percutaneous cardiovascular procedures with radial access versus femoral access in contemporary, real-world clinical settings.

Regional distribution and timing of wall motion abnormalities during echo-dipyridamole stress test in patients with stable angina: the elusive link between coronary stenoses and myocardial ischemia.

BACKGROUND: Classic experimental studies have shown that in the presence of a flow-limiting coronary artery stenosis, myocardial ischemia during metabolic or pharmacological arteriolar vasodilation causes wall motion abnormalities, which precede electrocardiographic (ECG) changes in the myocardial regions supplied by the stenotic branch. The aim of this study was to establish whether in patients with chronic stable angina the regional distribution of wall motion changes and sequence of ischemic events are similar to that observed in experimental models, as currently believed. METHODS: The study population consisted of 20 men and 4 women (mean age 59 +/- 10 years) who were recruited on the basis of the following criteria: 1) a history of chronic stable angina without clinical and instrumental evidence of previous myocardial infarction; 2) reproducible positive exercise tests for ECG myocardial ischemia and anginal pain; 3) angiographically normal left ventricular function; 4) isolated stenosis of the left anterior descending coronary artery (LAD). Patients underwent continuous 12-lead ECG and echocardiographic monitoring during dipyridamole infusion. RESULTS: During dipyridamole infusion 3 patients (13%) did not develop echocardiographic changes, ECG changes or angina, 14 (58%) exhibited ECG changes, 18 (75%) lamented angina and 16 (67%) developed echocardiographic changes. In 5 of these 16 patients (31.5%) echocardiographic changes occurred in LAD-dependent territories only, in 5 they occurred in non-LAD-dependent territories only (31.5%) and in 6 (37%) they occurred in both LAD- and non-LAD-dependent territories. A total of 14 patients exhibited both echocardiographic and ECG changes and/or angina. In 6 of these 14 patients (43%) echocardiographic changes were the first ischemic events; in the remaining 8 patients (57%) ECG changes and/or angina were the first ischemic events. CONCLUSION: In the majority of patients during dipyridamole infusion regional wall motion changes occur in territories supplied by non-stenotic coronary artery branches; they are probably caused, therefore, by distal vessel dysfunction. Furthermore, the sequence of ischemic events is different in individual patients. These findings indicate that in stable angina the mechanisms of ischemia are multiple and that the link between coronary stenoses and myocardial ischemia is very elusive.

Muscular and cardiac adenosine-induced pain is mediated by A1 receptors.

OBJECTIVES: This study attempted to establish whether bamiphylline, a selective antagonist of A1 adenosine receptors, prevents the algogenic effects of adenosine in humans. BACKGROUND: Experimental findings indicate that the sympathoexcitatory response elicited by adenosine is mediated by A1 receptors. METHODS: An intrailiac infusion of increasing doses (from 125 to 2,000 micrograms/min) of adenosine was given to 20 patients. Adenosine infusion was then repeated after intrailiac infusion of either bamiphylline or saline solution. In 14 other patients with angina, increasing doses of adenosine (from 108 to 1,728 micrograms/min) were infused into the left coronary artery. Adenosine infusion was then repeated after the intravenous infusion of either bamiphylline or placebo. Coronary blood flow velocity was monitored by a Doppler catheter. Data relative to pain severity are expressed as median and all other data as mean value +/- 1 SD. RESULTS: Bamiphylline prolonged the time to pain onset caused by the intrailiac adenosine infusion from 444 +/- 96 to 749 +/- 120 s (p < 0.001) and reduced pain severity from 45 to 24 mm (p < 0.01). After placebo infusion, the time to pain onset and pain severity were similar to that of baseline (428 +/- 112 vs. 430 +/- 104 s, p = 0.87 and 44 vs. 43 mm, p = 0.67, respectively). Bamiphylline prolonged the time to pain onset caused by intracoronary adenosine infusion from 519 +/- 128 to 603 +/- 146 s (p < 0.01) and reduced pain severity from 58 to 28 mm (p < 0.02). After placebo infusion, the time to pain onset and pain severity were similar to that at baseline (542 +/- 87 vs. 551 +/- 79 s, p = 0.14 and 55 vs. 50 mm, p = 0.61). Maximal coronary blood flow velocities before and after bamiphylline administration were similar (47 +/- 22 vs. 49 +/- 24 cm/s, p = 0.36) as well as before and after placebo administrtion (40 +/- 20 vs. 41 +/- 20 cm/s, p = 0.07). CONCLUSIONS: Bamiphylline reduces adenosine-induced muscular and cardiac pain but does not affect adenosine-induced coronary vasodilation. These findings indicate that at the dose used in this study, bamiphylline does not detectably block vascular A2-receptor-mediated adenosine effects in humans, which suggests that the muscular and cardiac algogenic effects of adenosine are mediated mainly by A1 receptors.

Right coronary artery cirsoid with fistulous connection to the coronary sinus.

A 61-yr-old woman was referred to our hospital for evaluation of a suspected right atrial myxoma. The transesophageal echocardiogram suggested the presence of an anomalous right coronary artery with fistulous connection to the coronary sinus. At cardiac catheterization, an oxygen step-up in the right atrium indicated a 1.3:1.0 left-to-right shunt. Aortic root angiography showed a large and calcified right coronary artery cirsoid draining to the coronary sinus, which appeared remarkably dilated. In this rare anomaly, cardiac catheterization is necessary, not only to quantify the magnitude of the left-to-right shunt, which is an important requirement for the indication to surgical treatment, but also to confirm the echocardiographic diagnosis.