Phospholemman deficiency in postinfarct hearts: enhanced contractility but increased mortality.

Phospholemman (PLM) regulates [Na(+) ](i), [Ca(2+)](i) and contractility through its interactions with Na(+)-K(+)-ATPase (NKA) and Na(+) /Ca(2+) exchanger (NCX1) in the heart. Both expression and phosphorylation of PLM are altered after myocardial infarction (MI) and heart failure. We tested the hypothesis that absence of PLM regulation of NKA and NCX1 in PLM-knockout (KO) mice is detrimental. Three weeks after MI, wild-type (WT) and PLM-KO hearts were similarly hypertrophied. PLM expression was lower but fractional phosphorylation was higher in WT-MI compared to WT-sham hearts. Left ventricular ejection fraction was severely depressed in WT-MI but significantly less depressed in PLM-KO-MI hearts despite similar infarct sizes. Compared with WT-sham myocytes, the abnormal [Ca(2+) ], transient and contraction amplitudes observed in WT-MI myocytes were ameliorated by genetic absence of PLM. In addition, NCX1 current was depressed in WT-MI but not in PLM-KO-MI myocytes. Despite improved myocardial and myocyte performance, PLM-KO mice demonstrated reduced survival after MI. Our findings indicate that alterations in PLM expression and phosphorylation are important adaptations post-MI, and that complete absence of PLM regulation of NKA and NCX1 is detrimental in post-MI animals.

Radial artery sterile granulomatous reaction secondary to hydrophilic-coated sheath used for transradial cardiac catheterization: a case series.

Radial access has lower risk of vascular complication for cardiac catheterization and is rapidly replacing femoral access. There are few unique complications associated with this approach. We present 3 cases of sterile granulomatous reaction associated with a specific hydrophilic radial sheath and possibly contribution by radial wrist band [TR band; Terumo Medical used for hemostasis after sheath removal (2101 cotton tail lane somerset NJ, USA)]. Awareness of this association will help clinicians use appropriate preventive measures.

Anginalike pain and normal coronary arteries. Uncovering cardiac syndromes that mimic CAD.

Atherosclerotic CAD is the most common cause of cardiac chest pain in Western countries. Other cardiac syndromes may also cause anginalike pain and may be difficult to differentiate from atherosclerotic CAD. It is essential to make this distinction, because management and prognosis of these conditions are entirely different. A detailed history and, in some cases, special diagnostic methods can help make the diagnosis. When evaluating patients with anginalike chest pain and normal coronary arteries, physicians need to consider this group of diseases and tailor workup and diagnosis on an individual basis.

Effects of phospholemman downregulation on contractility and [Ca(2+)]i transients in adult rat cardiac myocytes.

Phospholemman (PLM) expression was increased in rat hearts after myocardial infarction (MI). Overexpression of PLM in normal adult rat cardiac myocytes altered contractile function and cytosolic Ca(2+) concentration ([Ca(2+)](i)) homeostasis in a manner similar to that observed in post-MI myocytes. In this study, we tested whether PLM downregulation in normal adult rat myocytes resulted in contractility and [Ca(2+)](i) transient changes opposite to those observed in post-MI myocytes. Compared with control myocytes infected with adenovirus (Adv) expressing green fluorescent protein (GFP) alone, myocytes infected with Adv expressing both GFP and rat antisense PLM (rASPLM) had 23% less PLM protein (P < 0.012) at 3 days, but no differences were found in sarcoplasmic reticulum (SR) Ca(2+)-ATPase, Na(+)/Ca(2+) exchanger (NCX1), Na(+)-K(+)-ATPase, and calsequestrin levels. SR Ca(2+) uptake and whole cell capacitance were not affected by rASPLM treatment. Relaxation from caffeine-induced contracture was faster, and NCX1 current amplitudes were higher in rASPLM myocytes, indicating that PLM downregulation enhanced NCX1 activity. In native rat cardiac myocytes, coimmunoprecipitation experiments indicated an association of PLM with NCX1. At 0.6 mM [Ca(2+)](o), rASPLM myocytes had significantly (P < 0.003) lower contraction and [Ca(2+)](i) transient amplitudes than control GFP myocytes. At 5 mM [Ca(2+)](o), both contraction and [Ca(2+)](i) transient amplitudes were higher in rASPLM myocytes. This pattern of contractile and [Ca(2+)](i) transient behavior in rASPLM myocytes was opposite to that observed in post-MI rat myocytes. We conclude that downregulation of PLM in normal rat cardiac myocytes enhanced NCX1 function and affected [Ca(2+)](i) transient and contraction amplitudes. We suggest that PLM downregulation offers a potential therapeutic strategy for ameliorating contractile abnormalities in MI myocytes.