Acute Myocardial Infarction due to External Compression of the Left Main Coronary Artery by a Large Pulmonary Artery Aneurysm.

BACKGROUND: Although rare, external compression of the left main coronary artery (LMCA) by a pulmonary arterial aneurysm (PAA) as a consequence of pulmonary arterial hypertension causing stable angina pectoris is well described. However, acute myocardial infarction is extremely rare, particularly with a full array of electrocardiographic, biochemical, and echocardiographic features, as in this scenario. CASE: In this case, a 62-year-old man with a past history of severe fibrotic lung disease was hospitalised with chest pain. The patient had dynamic anterolateral ischaemic changes on electrocardiography and serially elevated high-sensitivity troponin I. Transthoracic echocardiography revealed impaired left ventricular ejection fraction with anterolateral hypokinesis. Coronary angiography with intracoronary imaging revealed external compression of the LMCA. Computer tomography (CT) scans confirmed new PAA, compared to previous scans. The patient was successfully treated by percutaneous coronary stent implantation. CONCLUSION: Progressive dilatation of the pulmonary artery due to pulmonary arterial hypertension can result in acute MI secondary to external compression of the LMCA. Clinicians should be mindful of acute coronary syndromes in patients with long-standing pulmonary hypertension presenting with chest pain.

Automated cardiopulmonary resuscitation using a load-distributing band external cardiac support device for in-hospital cardiac arrest: a single centre experience of AutoPulse-CPR.

BACKGROUND: Poor quality cardiopulmonary resuscitation (CPR) predicts adverse outcome. During invasive cardiac procedures automated-CPR (A-CPR) may help maintain effective resuscitation. The use of A-CPR following in-hospital cardiac arrest (IHCA) remains poorly described. AIMS & METHODS: Firstly, we aimed to assess the efficiency of healthcare staff using A-CPR in a cardiac arrest scenario at baseline, following re-training and over time (Scenario-based training). Secondly, we studied our clinical experience of A-CPR at our institution over a 2-year period, with particular emphasis on the details of invasive cardiac procedures performed, problems encountered, resuscitation rates and in-hospital outcome (AutoPulse-CPR Registry). RESULTS: Scenario-based training: Forty healthcare professionals were assessed. At baseline, time-to-position device was slow (mean 59 (±24) s (range 15-96s)), with the majority (57%) unable to mode-switch. Following re-training time-to-position reduced (28 (±9) s, p<0.01 vs baseline) with 95% able to mode-switch. This improvement was maintained over time. AutoPulse-CPR Registry: 285 patients suffered IHCA, 25 received A-CPR. Survival to hospital discharge following conventional CPR was 28/260 (11%) and 7/25 (28%) following A-CPR. A-CPR supported invasive procedures in 9 patients, 2 of whom had A-CPR dependant circulation during transfer to the catheter lab. CONCLUSION: A-CPR may provide excellent haemodynamic support and facilitate simultaneous invasive cardiac procedures. A significant learning curve exists when integrating A-CPR into clinical practice. Further studies are required to better define the role and effectiveness of A-CPR following IHCA.

Folate, homocysteine, endothelial function and cardiovascular disease. What is the link?

Elevated plasma homocysteine concentrations are associated with an increased risk of cardiovascular disease, but the relationship has not been proven to be causal. Folate is the strongest nutritional and pharmacological determinant of plasma homocysteine concentrations, which also interact with the genetic variation in methylenetetrahydrofolate reductase (MTHFR). Endothelial dysfunction due to reduced nitric oxide bioavailability is an early feature of vascular pathology. This can be assessed noninvasively by measurement of flow-mediated dilatation. Human studies on folic acid, homocysteine and endothelial function are reported. It is proposed that folic acid in high doses may have beneficial effects on endothelial function, which are independent of homocysteine lowering.

Flow-mediated dilatation following wrist and upper arm occlusion in humans: the contribution of nitric oxide.

Flow-mediated dilatation (FMD) of the brachial artery assessed by high-resolution ultrasound is widely used to measure endothelial function. However, the technique is not standardized, with different groups using occlusion of either the wrist or the upper arm to induce increased blood flow. The validity of the test as a marker of endothelial function rests on the assumption that the dilatation observed is endothelium-dependent and mediated by nitric oxide (NO). We sought to compare the NO component of brachial artery dilatation observed following wrist or upper arm occlusion. Dilatation was assessed before and during intra-arterial infusion of the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) following occlusion of (i) the wrist (distal to ultrasound probe) and (ii) the upper arm (proximal to ultrasound probe) for 5 min in ten healthy males. Dilatation was significantly greater after upper arm occlusion (upper arm, 11.62+/-3.17%; wrist, 7.25+/-2.49%; P=0.003). During L-NMMA infusion, dilatation after wrist occlusion was abolished (from 7.25+/-2.49% to 0.16+/-2.24%; P<0.001), whereas dilatation after upper arm occlusion was only partially attenuated (from 11.62+/-3.17% to 7.51+/-2.34%; P=0.006). The peak flow stimulus was similar after wrist and upper arm occlusion. We conclude that dilatation following upper arm occlusion is greater than that observed after wrist occlusion, despite a similar peak flow stimulus. L-NMMA infusion revealed that FMD following wrist occlusion is mediated exclusively by NO, while dilatation following upper arm occlusion comprises a substantial component not mediated by NO, most probably related to tissue ischaemia around the brachial artery. FMD following wrist occlusion may be a more valid marker of endothelial function than dilatation following upper arm occlusion.

Folate improves endothelial function in coronary artery disease: an effect mediated by reduction of intracellular superoxide?

Homocysteine is a risk factor for coronary artery disease (CAD). Folic acid lowers homocysteine and may improve endothelial function in CAD, although the mechanism is unclear. We investigated the effect of folic acid on endothelial function, homocysteine, and oxidative stress in patients with CAD. We also examined the acute effect of 5-methyltetrahydrofolate (5-MTHF), the principal circulating folate, on endothelial function in vivo and on intracellular superoxide in cultured endothelial cells. A randomized crossover study of folic acid (5 mg daily) for 6 weeks was undertaken in 52 patients with CAD. Ten further patients were given intra-arterial 5-MTHF. Endothelial function was assessed by flow-mediated dilatation (FMD). Folic acid increased plasma folate (P<0.001), lowered homocysteine by 19% (P<0.001), and improved FMD (P<0.001). FMD improvement did not correlate with homocysteine reduction. Malondialdehyde and total plasma antioxidant capacity, markers of oxidative stress, were unchanged. 5-MTHF acutely improved FMD (P<0.001) without altering homocysteine (P=0.47). In vitro, 5-MTHF abolished homocysteine-induced intracellular superoxide increase (P<0.001); this effect was also observed with folic acid and tetrahydrobiopterin. Our data support the beneficial effect of folic acid on endothelial function in CAD but suggest that the mechanism is independent of homocysteine. Reduction of intracellular endothelial superoxide may have contributed to the effect.