Monthly Archives: March 2013

Summary of Findings:

• 52yo M
• No known PMH
• Acute multifocal strokes (mostly cortical)
• Significant coronary atherosclerotic disease and a dilated LV with EF<25% and multi-wall hypokinesis
• Pulmonary emboli inflatable slide
• Mildly elevated troponins and significantly elevated lipoprotein A

LIPOPROTEIN A AND VENOUS THROMBOEMBOLISM

Elevated lipoprotein(a) [Lp(a)] levels are a recognized risk factor for cardiovascular disease. While some studies have shown that  an elevated Lp(a) level is an independent risk factor for venous thromboembolism in adultsAufblasbare Pools, suggesting that it may be involved in the pathogenesis of idiopathic and recurrent disease, other studies have found the risk of venous thromboembolism (VTE) in adults contradictory.princess playhouse bouncy castle

References:

1. Grifoni E, Marcucci R, Ciuti G, Cenci C, Poli D, Mannini L, Liotta AA, Miniati M, Abbate R, Prisco D. The thrombophilic pattern of different clinical manifestations of venous thromboembolism: a survey of 443 cases of venous thromboembolism. Semin Thromb Hemost. 2012 Mar;38(2):230-4
2. Marcucci R, Liotta AA, Cellai AP, Rogolino A, Gori AM, Giusti B, Poli D, Fedi S, Abbate R, Prisco D. Increased plasma levels of lipoprotein(a) and the risk of idiopathic and recurrent venous thromboembolism. Am J Med. 2003 Dec 1;115(8):601-5.

Case is courtesy of Claudio Smuclovisky, MD

This endomyocardial biopsy discloses a marked infiltrate of chronic inflammatory cells including lymphocytes, histiocytes, and eosinophils. Focally, the histiocytes appear to aggregate in poorly formed granulomas. Scattered multinucleated giant cells are present, some of which appear to be histiocytic and some of which appear to be muscle giant cells. This infiltrate does not have the typical appearance of sarcoidosis. No microorganisms or viral inclusions are identified. These changes are consistent with a diagnosis of giant cell myocarditis.

GIANT CELL MYOCARDITIS

• Giant cell myocarditis is a rare and highly lethal disorder that was first described by Saltykow in 1905
• Less than 300 cases have been reported in sub-sequent years
  • All GCM cases were either fatal or were managed with heart transplantation until 1987, when the successful treatment of GCM with triple drug immune suppression was reported
  • Autopsy studies conducted a number of years ago in England and Japan reported the incidence of GCM as 23.4 per 100,000 and 6.6 per 100,000
• GCM and cardiac sarcoidosis were historically grouped together. They have different clinical and histologic features
  • CS specimens had significantly more granulomas and fibrosis, while GCM had more necrosis and eosinophils
• GCM is usually an acute disease with rapid deterioration over weeks, while CS progresses over months to years
• Endomyocardial biopsy (EMB) should be considered in younger patients with idiopathic complete heart block to diagnose GCM or CS especially if a cardiomyopathy is present
• About MRI: “…not a perfect alternative because CMR information is less detailed and—in contrast to biopsy—does not allow to evaluate the exact degree of inflammation, the presence of special forms of myocarditis (such as giant cell or eosinophilic myocarditis which require specific therapies), or the presence and type of virus”

References:

1. Blauwet LA, Cooper LT. Idiopathic giant cell myocarditis and cardiac sarcoidosis. Heart Fail Rev. 2012 Oct 31.
2. Yilmaz A, Ferreira V, Klingel K, Kandolf R, Neubauer S, Sechtem U. Role of cardiovascular magnetic resonance imaging (CMR) in the diagnosis of acute and chronic myocarditis. Heart Fail Rev. 2012 Oct 18.
3. Cooper LT Jr, ElAmm C. Giant cell myocarditis. Diagnosis and treatment. Herz. 2012 Sep;37(6):632-6.

Case is courtesy of Travis S. Henry, MD.

Case #1:

52 y/o white male with no known past medical history had a syncopal episode at the local casino where he works and was brought to our Hospital. Had an initial CT followed by an MRA and MRI.

Echo: LV dilatation, EF 25% with multi wall hyokynesis.

Mildly elevated troponins and mild hyperlipidemia, lipoprotein A near 500, normal white count, hemoglobin:15,8, normal platelets, normal LFT’s, mild elevated ALT

INR: 0.94, normal renal function, glucose: 125.

Had a CCTA followed by a cardiac angio and CABG.

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