Brugada ECG pattern precipitated by acute pneumonia: a case report

Brugada type 1 ECG pattern is the hallmark for the diagnosis of Brugada syndrome which is a cause of sudden death due to ventricular arrhythmias. We present a case of a previously healthy young man who was admitted with productive cough with greenish phlegm and right-sided chest pain which was subsequently diagnosed as acute pneumonia. A routine ECG was done as part of his evaluation and showed Brugada ECG type 1 pattern. He was treated with antibiotics and on follow up his ECG was normal. In this report we present this increasingly described phenomenon and briefly review the literature

Steinert's syndrome presenting as anal incontinence: a case report

<p>Abstract</p> <p>Introduction</p> <p>Myotonic dystrophy (MD) or Steinert's syndrome is a rare cause of chronic diarrhea and anal incontinence. In the presence of chronic diarrhea and fecal incontinence with muscle weakness, neuromuscular disorders such as myotonic dystrophy should be considered in the differential diagnosis.</p> <p>Case Presentation</p> <p>We present the case of a 45-year-old Turkish man with Steinert's syndrome, who was not diagnosed until the age of 45.</p> <p>Conclusions</p> <p>In clinical practice, the persistence of diarrhea and fecal incontinence with muscle weakness should suggest that the physician perform an anal manometric study and electromyography. Neuromuscular disorders such as myotonic dystrophy should be considered in the differential diagnosis.</p

The predictive power of depression screening procedures for veterans with coronary artery disease

Stewart A Shankman1*, Jeffrey Nadelson2*, Sarah Kate McGowan1, Ali A Sovari2, Mladen I Vidovich21Department of Psychiatry and Psychology, University of Illinois, 2Department of Cardiology, Jesse Brown VA Medical Center, Chicago, IL, USA*These authors contributed equally to this workAbstract: Depression leads to a worse outcome for patients with coronary artery disease (CAD). Thus, accurately identifying depression in CAD patients is imperative. In many veterans affairs (VA) hospitals, patients are screened for depression once a year using the patient health questionnaire (PHQ-9). Although the PHQ-9 is generally considered a specific and sensitive measure of depression, there is reason to believe that these screening procedures may miss a large number of cases of depression within CAD patients and cardiology patients more generally. The goal of this study was to provide data as to the predictive power of this depression screening procedure by (a) comparing the prevalence rate of depression identified by the PHQ-9 to known prevalence rates and (b) examining whether patients identified as &amp;ldquo;depressed&amp;rdquo; also had conditions that consistently co-occur with depression (eg, post-traumatic stress disorder [PTSD], other medical issues). Participants were 813 consecutive patients who received an angiogram in the cardiac catheterization laboratory at a large VA Medical Center. Prevalence of depression was 6.9% in the overall sample and less than 6% when the sample was restricted to CAD patients with significant stenosis. Depression was significantly associated with PTSD, smoking, and alcohol problems. However, depression was not associated with other medical problems such as diabetes, renal failure, peripheral vascular disease, or anemia. In conclusion, the low prevalence rate of depression and lack of associations with comorbid medical problems may suggest that the VA&amp;rsquo;s depression screening procedures have low sensitivity for identifying depression in CAD patients. It is recommended that clinicians treating CAD regularly screen for depression and do not rely on archival depression screens.Keywords: depression screening, coronary artery disease, PHQ-9, veteran

Induction of Atrial Fibrillation by Neutrophils Critically Depends on CD11b/CD18 Integrins

Background: Recent observational clinical and ex-vivo studies suggest that inflammation and in particular leukocyte activation predisposes to atrial fibrillation (AF). However, whether local binding and extravasation of leukocytes into atrial myocardium is an essential prerequisite for the initiation and propagation of AF remains elusive. Here we investigated the role of atrial CD11b/CD18 mediated infiltration of polymorphonuclear neutrophils (PMN) for the susceptibility to AF. Methods and Results: C57bl/6J wildtype (WT) and CD11b/CD18 knock-out (CD11b(-/-)) mice were treated for 14 days with subcutaneous infusion of angiotensin II (Ang II), a known stimulus for PMN activation. Atria of Ang II-treated WT mice were characterized by increased PMN infiltration assessed in immunohistochemically stained sections. In contrast, atrial sections of CD11b(-/-) mice lacked a significant increase in PMN infiltration upon Ang II infusion. PMN infiltration was accompanied by profoundly enhanced atrial fibrosis in Ang II treated WT as compared to CD11b(-/-) mice. Upon in-vivo electrophysiological investigation, Ang II treatment significantly elevated the susceptibility for AF in WT mice if compared to vehicle treated animals given an increased number and increased duration of AF episodes. In contrast, animals deficient of CD11b/CD18 were entirely protected from AF induction. Likewise, epicardial activation mapping revealed decreased electrical conduction velocity in atria of Ang II treated WT mice, which was preserved in CD11b(-/-) mice. In addition, atrial PMN infiltration was enhanced in atrial appendage sections of patients with persistent AF as compared to patients without AF. Conclusions: The current data critically link CD11b-integrin mediated atrial PMN infiltration to the formation of fibrosis, which promotes the initiation and propagation of AF. These findings not only reveal a mechanistic role of leukocytes in AF but also point towards a potential novel avenue of treatment in AF

Tumor Necrosis Factor - Alpha Is Essential for Angiotensin II-Induced Ventricular Remodeling: Role for Oxidative Stress

The functional crosstalk between angiotensin II (Ang II) and tumor necrosis factor (TNF)-α has been shown to cause adverse left ventricular remodeling and hypertrophy in hypertension. Previous studies from our lab showed that mice lacking TNF-α (TNF-α-/-) have attenuated hypertensive response to Ang II; however, the signaling mechanisms involved are not known. In this study, we investigated the signaling pathways involved in the Ang II and TNF-α interaction. Chronic Ang II infusion (1 μg/kg/min, 14 days) significantly increased cardiac collagen I, collagen III, CTGF and TGF-β mRNA and protein expression in wild-type (WT) mice, whereas these changes were decreased in TNF-α-/- mice. TNF-α-/- mice with Ang II infusion showed reduced myocardial perivascular and interstitial fibrosis compared to WT mice with Ang II infusion. In WT mice, Ang II infusion increased reactive oxygen species formation and the expression of NADPH oxidase subunits, indicating increased oxidative stress, but not in TNF-α-/- mice. In addition, treatment with etanercept (8 mg/kg, every 3 days) for two weeks blunted the Ang II-induced hypertension (133 ± 4 vs 154 ± 3 mmHg, p<0.05) and cardiac hypertrophy (heart weight to body weight ratio, 4.8 ± 0.2 vs 5.6 ± 0.3, p<0.05) in WT mice. Furthermore, Ang II-induced activation of NF-κB, p38 MAPK, and JNK were reduced in both TNF-α-/- mice and mice treated with etanercept. Together, these findings indicate that TNF-α contributes to Ang II-induced hypertension and adverse cardiac remodeling, and that these effects are associated with changes in the oxidative stress dependent MAPK/TGF-β/NF-κB pathway. These results may provide new insight into the mechanisms of Ang II and TNF-α interaction