Jaber Sawaya

Traumatic pseudoaneurysm of the left sinus of Valsalva: a case report.

Deceleration injuries of the aorta result in tears that often lead to exsanguinating hemorrhage. The site is most often at the aortic isthmus, with injuries of the aortic root being rare. A minority of patients survive long enough to reach the hospital where prompt diagnosis and treatment are essential for survival. We hereby report on a patient who had a pseudoaneurysm of the left sinus of Valsalva 13 years after a deceleration accident, presumably caused by a contained rupture of the aortic root. Transesophageal echocardiography was of great value in studying the features of the pseudoaneurysm and its relation to the left main coronary artery and left upper pulmonary vein.

Comparison of the systemic levels of inflammatory markers after percutaneous coronary intervention with bare metal versus sirolimus-eluting stents.

BACKGROUND Percutaneous coronary intervention (PCI) with bare metal stent (BMS) deployment causes plaque disruption and a rise in systemic levels of C-reactive protein (CRP), interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1. Our aim is to study whether PCI with sirolimus-eluting stent (SES) use attenuates this response. METHODS Patients with stable angina undergoing single-vessel PCI were enrolled in a randomized, open-label fashion into a BMS group or an SES group. Blood samples were drawn pre-PCI, 24 hours post-PCI, and 30 days post-PCI. Systemic concentrations of CRP, IL-6, and MCP-1 were measured at all time points. RESULTS In total, 41 patients were enrolled (21 in the BMS group and 20 in the SES group). The baseline plasma concentrations of all markers were comparable between groups. At 24 hours, the mean plasma CRP concentration in the SES group was 20.21 mg/dL versus 8.95 mg/dL in the BMS group (P = 0.15). The mean plasma IL-6 concentration at 24 hours was 25.41 pg/mL in the SES group versus 17.44 pg/mL in the BMS group (P = 0.17). The mean plasma MCP-1 concentration at 24 hours was 382.38 pg/mL in the SES group versus 329.04 pg/mL in the BMS group (P = 0.2). At 30 days, plasma concentrations of all three markers decreased to similar values between groups. CONCLUSIONS The use of SES did not inhibit the rise in systemic concentrations of CRP, IL-6, and MCP-1 at 24 hours or 30 days post-PCI, compared with BMS. Moreover, at 24 hours, there was a trend for higher systemic levels of all proinflammatory markers in the SES group compared with the BMS cohort.

Cardiac tamponade caused by polymicrobial Gram-negative organisms

Polymicrobial gram-negative pericarditis is a rare entity. We describe the first case of suppurative pericarditis with Citrobacter diversus and Proteus mirabilis.

Early diagnosis of pericarditis in acute myocardial infarction

Pericarditis complicating acute myocardial infarction assumes increasing importance in this era of quantitating infarct size by precordial ST segment mapping. Early recognition of this complication avoids diagnostic and therapeutic errors. In this study we looked for factors that could alert to the early diagnosis of pericarditis, such as ST elevation measured within 24 hours from onset, extent of CPK, LDH, and SGOT elevation, as well as degree of pump dysfunction. ST segment elevation in millimeters on admission seemed to be one factor that was of predictive value in this condition. Pericarditis occurred in three forms: (1) within a few hours from the onset of myocardial infarction and this form seems to carry a high mortality rate; (2) a more common variety occurs within 24 to 72 hours from onset and carries a higher mortality rate than matched controls; and (3) the late syndrome of Dresslers, not observed in our series. Aside from increased incidence of heart failure, other complications of myocardial infarction and the coronary risk factors were not significantly higher in patients with pericarditis. Salicylate treatment offers immediate relief in the majority of patients.

The i allele of the angiotensin converting enzyme I/D polymorphism confers protection against coronary artery disease

BackgroundMutations in genes regulating lipid metabolism, vasoactivity, and coagulation are important modulators of coronary artery disease (CAD). ObjectiveThis study investigated the association between allelic variants of the angiotensin converting enzyme (ACE), methytetrahydrofolate reductase, plasminogen activator inhibitor-1 and factor V genes and CAD. MethodsClinical, biochemical, and angiographic information were collected from 300 patients who underwent cardiac catheterization and their DNA was genotyped by restriction fragment length polymorphism. ResultsThe frequency of the D allele of the ACE gene was significantly higher than the I allele in patients with more than 70% stenosis in any vessel. Among patients with more than 70% stenosis, carriers of the D allele were 2.8 times more likely to be males. The presence of the ACE I allele was negatively associated with CAD with (P=0.02 ,OR=0.38.) ConclusionThis study describes a protective role of the ACE I allele in individuals who may be at risk of developing CAD.

Asymptomatic Spontaneous Coronary Artery Dissection

Spontaneous coronary artery dissection (SCAD) is a rare cause of myocardial ischemia that could present as angina, acute myocardial infarction, or even sudden death. It occurs more commonly in women and it has been associated with autoimmune and collagen vascular diseases. The management and prognosis in these patients depend on the initial clinical presentation and the extent of dissection. In this article, we report 2 cases of asymptomatic SCAD that were diagnosed on routine preoperative evaluation. The management options and clinical implications are discussed. Copyright

Acute myocardial infarction in a young man: A consequence of inherited thrombophilia and marijuana smoking

Acute myocardial infarction in a young man: A consequence of inherited thrombophilia and marijuana smoking -

Switching patients from warfarin to dabigatran therapy: To RE-LY or not to rely☆

The RE-LY study showed that dabigatran, given at 110 mg twice daily, is non-inferior to warfarin for preventing stroke in patients with atrial fibrillation [1]. Previous vitamin K antagonist exposure was also shown not to influence the benefits of dabigatran in this setting [2]. We herein present an unfavorable outcome after shifting an eligible patient from warfarin to dabigatran therapy; thus challenging some existing comfort zones. A 78-year-old, 80-kg patient with controlled hypertension underwent angioplasty and Cypher stent implantation in the proximal Ramus artery five years ago; and has been free of coronary events since then. One year after stent placement, the patient underwent laparoscopic cholecystectomy at which time he was noted to be in sinus rhythm. One year later and on routine evaluation, he was found to be in atrial fibrillation. Transesophageal echocardiogram showed a left atrial thrombus (Fig. 1A) and the patient was started on warfarin therapy with close follow-up of prothrombin time being in the therapeutic range. Repeat echocardiogram one year later showed the left atrium to be free of thrombus (Fig. 1B). Following data from the

Viagra, Sexual Intercourse and Acute Myocardial Infarction

Accessible online at: www.karger.com/journals/crd Dear Sir, Viagra (sildenafil) is a new drug approved for the treatment of erectile dysfunction. It increases the concentration of cyclic guanosine monophosphate in the smooth muscle cells of the corpora cavernosa leading to vasodilatation and increased penile response to sexual stimulation [1]. We report a patient that sustained an acute myocardial infarction after taking Viagra and performing sexual intercourse. A 51-year-old patient presented to the hospital complaining of severe chest pain that started 1 h after taking a tablet of Viagra (for the first time) and performing sexual intercourse. His blood pressure and pulse rate were 105/65 mm Hg and 74 beats/min, respectively. Physical examination was normal. Electrocardiogram done on admission showed acute inferior myocardial infarction for which he received 100 mg of tissue plasminogen activator. The patient is known to have hyperlipidemia and coronary artery disease from 2 years ago when he underwent coronary angiography, for an episode of chest pain, which showed a 70% stenosis in the diagonal branch, 40% stenosis in the distal circumflex artery, and 30% stenosis in the mid-right coronary artery. He was treated with aspirin and simvastatin and remained asymptomatic until his current hospitalization. His course in the hospital during this admission was uncomplicated. His peak creatine kinase and creatine kinase-MB were 643 and 34 U/l, respectively. Echocardiography showed a hypokinetic inferior wall with an ejection fraction of 45%. Coronary angiography revealed a 100% occluded right coronary artery receiving collaterals from the left coronary artery. There was no significant change in the angiographic findings in the left coronary artery from 2 years ago. It is estimated that more than five million prescriptions for Viagra have already been filled worldwide. Our patient had his myocardial infarction after taking Viagra and performing sexual intercourse. Thus, this coronary event could be due to Viagra, the physical exertion of sexual intercourse or a combination of both factors. An association between Viagra intake and acute myocardial infarction has been reported [2]. In addition, the US Food and Drug Administration has received 69 reports of deaths in people taking Viagra between March and July 1998 [3]. The recently published ‘ACC/ AHA Expert Consensus Document’ states that the cardiovascular effects of Viagra may be potentially hazardous in patients with active coronary ischemia [4]. Our report suggests that the use of Viagra in patients with underlying coronary artery disease might be hazardous even if they are currently asymptomatic. As the use of Viagra among men increases, careful screening of patients becomes essential to ensure its safety especially in patients with underlying coronary artery disease.