Left ventricular decompression through a patent foramen ovale in a patient with hypertrophic cardiomyopathy: a case report

The foramen ovale is considered an unidirectional flap-like valvular structure. Yet, it may increase in size and allow a continuous left-to-right shunt in order to reduce left ventricular filling pressures. We report the case of a 63-year-old woman with hypertrophic cardiomyopathy, referred for percutaneous closure of a coexisting secundum atrial septal defect. Before catheterization, however, transesophageal echocardiography revealed a continuous left-to-right shunt within the atrial septum, thus suggesting the diagnosis of patent foramen ovale with stable left-to-right shunt. At catheterization, performed under general anesthesia and transesophageal echocardiographic monitoring, left ventricular early- and end-diastolic pressures were 2 and 12 mmHg and pulmonary-to-systemic flow ratio was 1.4. Provocative maneuvers were not able to reverse the shunt. In order to assess the effect of the increased left ventricular preload due to the abolition of the shunt, an Amplatzer sizing balloon was inflated for 5 minutes across the patent foramen ovale. Diastolic pressures rose up to 5 and 18 mmHg, respectively. Such a worsening of left ventricular function suggested us not to perform the closure procedure. Transcatheter closure of any interatrial communication with stable left-to-right shunt induces an abrupt overload of the left ventricle that may cause acute heart failure in patients with coexisting left ventricular dysfunction. The hemodynamic evaluation of left ventricular function during transient abolition of the shunt is an useful tool in order to establish the most correct therapeutic strategy. The closure procedure should not be performed if a worsening of left ventricular function occurs

Interplay between COVID-19, pollution, and weather features on changes in the incidence of acute coronary syndromes in early 2020

Coronavirus disease 2019 (COVID-19) has caused an unprecedented change in the apparent epidemiology of acute coronary syndromes (ACS). However, the interplay between this disease, changes in pollution, climate, and aversion to activation of emergency medical services represents a challenging conundrum. We aimed at appraising the impact of COVID-19, weather, and environment features on the occurrence of ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) in a large Italian region and metropolitan area

Reply: Bioresorbable Scaffolds in Cardiac Allograft Vasculopathy-Searching for the Holy Grail Facing the challenge of the "Perilous Seat"

No abstract availabl

Revascularization strategies in patients with combined carotid and coronary artery disease

A direct comparison of early and late outcomes with three approaches to carotid revascularization and open heart surgery

C-Reactive protein, clinical outcome, and restenosis rates after implantation of different drug-eluting stents

Sirolimus-eluting stents (SESs), paclitaxel-eluting stents (PESs), and dexamethasoneeluting stents (DEXs) have anti-inflammatory properties; thus, the decreased in-segment restenosis rate observed with the use of these stents might be related to a weaker postprocedural inflammatory response. One hundred sixty consecutive patients with stable coronary artery disease who underwent successful single-vessel/ lesion coronary artery stenting were prospectively studied. Thin-strut bare metal stents were. deployed in 39 patients, SESs in 30, PESs in 61, and DEXs in 30. The 4 groups were similar with respect to demographic and angiographic variables and prevalence of risk factors. C-reactive protein (CRP) was measured at baseline and 24 and 48 hours after the procedure. Maximal increase in CRP was calculated as the increase in CRP at 48 hours/CRP compared with baseline. Angiographic follow-up was performed after 12.9 +/- 1.3 months or sooner, if needed, on the basis of clinical evidence. All patients presented a postprocedural increase in CRP that peaked at 48 hours (median 10.0 mg/L). Maximal CRP increase was similar across the 4 groups (medians 3.5 mg/L in the bare metal stent group, 3.6 mg/L in the SES group, 4.0 mg/L in the PES group, 3.5 mg/L in the DEX group, p = 0.45). Incidences of angiographic binary restenosis (> 50% lumen diameter decrease) were 20.5% in the bare metal stent group, 3.3% in the SES group, 4.9% in the PES group, and 36.6% in the DEX group (p = 0.0004 for SES and PES groups vs bare metal stent and DEX groups). Post-procedural increase in CRP was significantly correlated with clinical and angiographic outcomes. In conclusion, the acute postprocedural systemic inflammatory response induced by drug-eluting stent implantation appears to be similar to that induced by bare metal stents. However, the restenosis rate is lower for SESs and PESs than for DEXs and bare metal stents. Thus, the decreased incidence of stent restenosis that was observed after SES and PES deployment is unlikely to be related to a decreased acute systemic inflammatory response, but rather to an increased local resistance to inflammatory mediators. (c) 2006 Elsevier Inc. All rights reserved

Muscular and cardiac adenosine-induced pain is mediated by A1receptors

AbstractObjectives. This study attempted to establish whether bamiphylline, a selective antagonist of A1adenosine receptors, prevents the algogenic effects of adenosine in humans.Background. Experimental findings indicate that the sympathoexcitatory response elicited by adenosine is mediated by A1receptors.Methods. An intrailiac infusion of increasing doses (from 125 to 2,000 μg/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 μg/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 administration (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 A1receptors