Henry C. Quevedo

Natural Disasters and Myocardial Infarction: The Six Years After Hurricane Katrina

OBJECTIVE To determine the prolonged effect of Hurricane Katrina on the incidence and timing of acute myocardial infarction (AMI) in the city of New Orleans. PATIENTS AND METHODS Our study population consisted of 1476 patients with AMI before (August 29, 1999, to August 28, 2005) and after (February 14, 2006, to February 13, 2012) Hurricane Katrina at Tulane University Health Sciences Center to determine post-Katrina alterations in the occurrence and timing of AMI. RESULTS Compared with pre-Katrina values, there was a more than 3-fold increase in the percentage of admissions for AMI during the 6 years after Hurricane Katrina (P<.001). The percentage of admissions for AMI after Hurricane Katrina increased significantly on nights (P<.001) and weekends (P<.001) and decreased significantly on mornings (P<.001), Mondays (P<.001), and weekdays (P<.001). Patients with AMI after Hurricane Katrina also had significantly higher rates of psychiatric comorbidities (P=.01), smoking (P<.001), lack of health insurance (P<.05), and unemployment (P<.001). CONCLUSION These results indicate that the effect of natural disasters on the occurrence of AMI may persist for at least a 6-year period and may be related to various factors including population shifts, alterations in the health care system, and the effects of chronic stress and associated behaviors.

Occurrence of Takotsubo cardiomyopathy and use of antidepressants

Takotsubo cardiomyopathy (TTC), also known as stress-induced cardiomyopathy, is a peculiar reversible cardiovascular disease (CVD) that may mimic an acute coronary syndrome, often affecting postmenopausal women after a stressful event. The prevalence ranges between 1.7 and 2.2% inpatients admittedwith chest pain for suspected acute coronary syndrome [1,2]. Proposed pathophysiological mechanisms include: catecholamine cardiotoxicity, microvascular dysfunction and coronary artery spasm [3,4]. Major depression and comorbid anxiety disorders have been associated with elevated sympathetic activity and diminished reuptake of norepinephrine, which may be responsible for prolonged cardiac sympathetic stimulation [5]. As suggested by Ziegelstein et al. [6], the double impact effect of disproportional high catecholamine responses and increased cardiac sympathetic sensitivity may place depressed patients at higher risk for developing TTC when exposed to stressful situations. Several case reports [7–11] have suggested that the use of SSRIs (in both therapeutic and over dosage scenarios) is associated with TCC, potentially by increasing norepinephrine levels in neuronal tissue via reuptake inhibition. This retrospective descriptive study consisted of 78 patients who met the Modified Mayo criteria [12]: 1) akinesia or dyskinesia of the apical and/or midventricular segments of the left ventricle with regionalwallmotionabnormalities extendingbeyond thedistributionof a single epicardial vessel, 2) absence of obstructive coronary artery disease, 3) new electrocardiographic abnormalities, and 4) absence of pheochromocytomas/myocarditis. The diagnosis of depression and anxiety was made based on clinical criteria by a primary care physician or psychiatrist before being admitted to the hospital. The diagnosis of anxiety included generalized anxiety disorder, panic disorder, post-traumatic stress disorder and social phobia. Clinical outcomes were assessed during the hospital admission and within 6 months after the index event, as follows: in hospital death (all cause-mortality), inpatient acute heart failure (HF), length of stay, and left ventricular ejection fraction (LVEF) determined by 2-D echocardiogram. Chi-squared and paired t-tests were used to assess statistical differences in categorical and continuous variables, respectively. A twotailed P b 0.05 was considered statistical significant. Cox-proportional hazard model was constructed to evaluate mortality. All analyses were performed employing SPSS v 19.0, Chicago IL. This study was approved by the hospital’s institutional review board. Baseline characteristics of the studypopulation aswell as by SSRI use are reported in Tables 1 and 2 respectively. SSRIs use was strongly associatedwith all-causemortality during index hospital admission (OR 7.6; 95% CI 1.1–50.3; P= 0.016). Mean LVEF on admission in patients taking SSRIs was 36.3 ± 11.4% and for patients not taking SSRIs was 36.7 ± 11.0%. Repeated echocardiogram within 6-months revealed statistically significant recovery of LVEF in each group (P b 0.05 for both comparisons) with a relatively lower LVEF in patients taking SSRIs (Fig. 1, P = 0.01). (See Table 3.) Mean LVEF on admission for patients without depressionwas 36.4 ± 11.2% and for patients with depression was 37.2 ± 10.6%. Repeated LVEF within 6-months revealed statistically significant recovery of LVEF in each group (P b 0.05 for both comparisons), although patientswith depression had relatively lower LVEFcompared topatientswithoutdepression (Fig. 2, P=0.02). The survival curve (Fig. 3) showed that SSRIs patients had lower survival rate compared with patients not taking SSRIs (P=0.04). In this study, the prevalence of depression and anxiety (21% and 31%, respectively) was consistent with previous reports [4,13,14] which reported a prevalence ranging between 20 and 40%. Several authors

Succesful antegrade subintimal bypass restenting of in-stent chronic total occlusion.

Coronary chronic total occlusions (CTOs) are known to cause significant patient morbidity. Over the past several years, the techniques and devices for treating these CTOs have advanced tremendously. The interventional management of CTOs within previously placed coronary stents, however, remains challenging. Here, we present a case of an in‐stent restenosis of the right coronary artery CTO bypassed using a controlled subintimal dissection re‐entry technique via antegrade approach creating side‐by‐side stents.

Endovascular therapy for ascending aorta pseudoaneurysm

Ascending Aortic pseudoaneurysms (AAP) are often formed as a result of prior thoracic surgery. In patients with large AAP, surgical correction is the established therapy. However, a group of patients are not suitable surgical candidates because of advanced age or multiple comorbidities. Instead, endovascular approach represents a viable option in this population. Here, we review the literature of the surgical and trans-catheter therapy for AAP. Additionally, we complement the review with a case presentation of a prohibitive surgical risk case that was treated with endovascular options including an unsuccessful septal occluder deployment, but final excellent angiographic AAP exclusion with coil embolization.

Coronary Vasospasm While Treating Supraventricular Tachycardia: Is Adenosine Really to Blame?

Coronary artery spasm has been reported during adenosine stress testing. Herein, we describe a transient ST-segment elevation following adenosine therapy for supraventricular tachycardia. A 38-year-old male presented to the emergency department with palpitations. Electrocardiogram showed supraventricular tachycardia with short RP interval. Vagal maneuvers were unsuccessful. Adenosine was then administered in two successive injections of 6 and 12 mg dosages, respectively. A subsequent 12-lead electrocardiogram revealed ST-segment elevation in inferior leads with reciprocal changes. Coronary angiography disclosed nonobstructive coronary disease. A postprocedure electrocardiogram exhibited normal sinus rhythm with nonspecific T wave abnormalities. Cardiac biomarkers were elevated with a peak troponin I of 0.32. Echocardiogram depicted bicuspid aortic valve and normal systolic function. Electrophysiological study revealed a concealed left accessory pathway and successful radiofrequency ablation was performed. Given the dynamic changes in the electrocardiogram, we hypothesize that this event was most likely a coronary vasospasm. The mechanism of coronary spasm following adenosine injection remains uncertain. Potential mediators include KATP channels and adenosine-2 receptors.

Simultaneous right ventricular to pulmonary artery pressure gradient measurement using a single venous access technique

Purpose The pullback gradient technique is commonly used to evaluate pulmonic stenosis; however, it only represents a one-time measurement of valvular stenosis. Instead, simultaneous peak-to-peak gradients account for the data variability being best suited to discern the severity of the stenosis, but requires two different venous accesses. Here, we demonstrate the feasibility and high fidelity hemodynamic tracings of a new technique for evaluation of pulmonary valve stenosis by using a single venous access. Methods We present a patient scenario suggesting pulmonic stenosis. Given the possible therapeutic intervention, we decided to use a single large bore (8-French) venous access. Results Simultaneous peak-to-peak gradients were obtained from high fidelity hemodynamic tracings measured using two small-size catheters located in the right ventricle (RV) and pulmonary artery (PA), respectively. The procedure had no complications. Conclusions We present a technique using single venous access for simultaneous RV and PA pressure measurement that is easy to perform and, importantly, it may be safer than exposing the patient to multiple venous accesses.

Pacemaker Lead Entrapment Complicating Transcatheter Closure of a Patent Foramen Ovale

Transcatheter cardiovascular interventions are nowadays more frequently and safely performed, thus leading to populate the heart with medical devices. Here, we describe an unusual complication following percutaneous closure of a patent foramen ovale (PFO) with an atrial septal occluder. A 52-year-