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J Am Coll Cardiol, 2007; 49:31-32, doi:10.1016/S0735-1097(07)01667-1
© 2007 by the American College of Cardiology Foundation
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INSIDE THIS ISSUE OF JACC

Inside this Issue of JACC


    Interventional Cardiology
 Top
 Interventional Cardiology
 Heart Rhythm Disorders
 Cardiomyopathy
 Cardiomyopathy
 Preclinical Study
 
Relieving Ischemia With PCI Reduces BNP Levels.  
Figure 1
While left ventricular (LV) dysfunction is known to be associated with increased plasma natriuretic peptide concentrations, the effect of intermittent ischemia on B-type natriuretic peptide (BNP) levels is unknown. McClure and colleagues systematically studied 26 patients with stable angina, normal LV systolic function, and isolated stenoses of the left anterior descending. Eight weeks after revascularization, 24 patients demonstrated significant decreases in plasma BNP. The mean decrease was equivalent to a 59% reduction, with no significant change in LV systolic function. This study suggests that recurrent ischemia may promote BNP release. See page 2394 . See figure.


    Heart Rhythm Disorders
 Top
 Interventional Cardiology
 Heart Rhythm Disorders
 Cardiomyopathy
 Cardiomyopathy
 Preclinical Study
 
Effects of Age, Gender, and Comorbidities on Survival in Patients With ICDs.  
Figure 2
Lee and colleagues hypothesized that recipient age, gender, and medical comorbidities may significantly effect outcomes in implantable cardioverter-defibrillator (ICD) recipients. They reviewed records from almost 2,500 ICD recipients. Older age at implant increased the risk of death; those 65 to 74 years of age were twice as likely to die as those <65 years of age. Recipients >75 years of age were 3 times as likely to die. Noncardiac conditions associated with increased risk of death included peripheral vascular disease, pulmonary disease, and renal disease. Age and noncardiac comorbidities significantly influence survival in ICD recipients; these factors should be considered when identifying patients likely to benefit from ICD implantation. See page 2408 . See figure.


    Cardiomyopathy
 Top
 Interventional Cardiology
 Heart Rhythm Disorders
 Cardiomyopathy
 Cardiomyopathy
 Preclinical Study
 
Characteristics of a Novel Phenotype of HCM.   Kubo and colleagues have noted that a certain percentage of their patients with clinical characteristics of hypertrophic cardiomyopathy (HCM) do not manifest left ventricular hypertrophy but do have a ’restrictive phenotype’ and evidence of myocyte disarray at autopsy. In a review of over 1,000 patients or family members of patients with HCM, 19 patients with a restrictive phenotype were identified. The 5-year survival rate for these patients was worse than for those with HCM. While mutations were found in the genes for several sarcomere proteins, those in the beta-myosin heavy chain and cardiac troponin I were more likely related to the phenotype. Restrictive phenotype HCM is a rare variant of HCM that seems to preclude a worse clinical course despite the lack of the eponymous hypertrophy. See page 2419.


    Cardiomyopathy
 Top
 Interventional Cardiology
 Heart Rhythm Disorders
 Cardiomyopathy
 Cardiomyopathy
 Preclinical Study
 
Mutation in Lamin Gene Leads to Severe Myocardial Fibrosis.  
Figure 3
Van Tintelen and colleagues have identified a large family with an autosomal dominantly inherited form of myocardial fibrosis. Twenty-five family members were clinically evaluated, including deoxyribonucleic acid and endomyocardial biopsy samples. Linkage disequilibrium suggested the region of the lamin AC (LMNA) gene. These proteins are major components of the nuclear lamina, a fibrous network underlying the inner surface of the nuclear envelope. Subsequent investigations showed that the genetic defect was a deletion of the start codon for the gene. This novel LMNA deletion causes a distinct, highly malignant cardiomyopathy with early-onset cardiac fibrosis. See page 2430 . See figure.


    Preclinical Study
 Top
 Interventional Cardiology
 Heart Rhythm Disorders
 Cardiomyopathy
 Cardiomyopathy
 Preclinical Study
 
Iron Potentiates the Cardiotoxicity of Doxorubicin.  
Figure 4
Doxorubicin (DOX) is known to form a complex with iron which may speed the transfer of electrons to molecular oxygen to generate highly reactive oxygen radicals. Panjrath and colleagues studied the interaction between DOX and iron in a rat model. In a 2 x 2 randomization scheme, rats were randomized to a diet rich in iron or standard chow, and to DOX or placebo. Animals fed iron-rich chow showed significantly higher DOX cardiotoxicity as evidenced by greater weight loss, more severe myocyte injury on electron microscopy, and increased cleaved caspase-3 staining. Feeding iron-rich chow alone did not result in any cardiotoxicity. This study suggests that iron potentiates the cardiotoxicity of DOX, presumably by generating free radials. See page 2457 . See figure.


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Severe Myocardial Fibrosis Caused by a Deletion of the 5’ End of the Lamin A/C Gene
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