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  • Effect of Moderate-Intensity Exercise Training on Peak Oxygen Consumption in Patients With Hypertrophic Cardiomyopathy: A Randomized Clinical Trial

    Abstract Full Text
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    JAMA. 2017; 317(13):1349-1357. doi: 10.1001/jama.2017.2503

    This randomized clinical trial assesses whether moderate-intensity exercise training, compared with usual activity, improves exercise capacity in adults with hypertrophic cardiomyopathy.

  • Recreational Exercise in Hypertrophic Cardiomyopathy

    Abstract Full Text
    JAMA. 2017; 317(13):1319-1320. doi: 10.1001/jama.2017.2584
  • Noncoding RNA May Help Treat Heart Disease

    Abstract Full Text
    JAMA. 2016; 315(13):1327-1327. doi: 10.1001/jama.2016.3236
  • JAMA December 9, 2009

    Figure 2: Pedigree for Hypertrophic Cardiomyopathy (HCM) Family

    Results of genetic testing are shown for family members who had this testing. P in p.G82R indicates protein. Documented evaluation (ie, echocardiography or electrocardiography) yielded results for normal left ventricular wall thickness (white) or hypertrophic cardiomyopathy (black).
  • JAMA October 21, 2009

    Figure 2: Phenotypes of Hypertrophic Cardiomyopathy

    Cross-sectional short axis magnetic resonance images. Top left, In the donor, segmental hypertrophy involving the posterior (inferior) free wall of the left ventricle (LV) and small contiguous portion of ventricular septum (VS) in the mid-LV cavity at papillary muscle level (black asterisk, 18-mm thickness) and also extending into the adjacent right ventricular (RV) wall (black arrowheads). Top right, Confluent midmyocardial (and transmural) delayed enhancement in the region of hypertrophy (dotted ellipse) and posterior papillary muscle (black arrowhead).Bottom left, In a 14-year-old male offspring, the distribution of LV cavity hypertrophy is almost identical to that in the donor (see top left), with marked segmental hypertrophy involving posterior (inferior) septum and contiguous posterior free wall at papillary muscle level (black asterisk, 30-mm thickness). Bottom right, Absence of delayed enhancement.
  • Implications of Hypertrophic Cardiomyopathy Transmitted by Sperm Donation

    Abstract Full Text
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    JAMA. 2009; 302(15):1681-1684. doi: 10.1001/jama.2009.1507
  • Hypertrophic Cardiomyopathy

    Abstract Full Text
    JAMA. 2009; 302(15):1720-1720. doi: 10.1001/jama.302.15.1720
  • JAMA October 21, 2009

    Figure 1: Pedigree Showing Offspring of the Sperm Donor

    In the 2 genetically affected offspring without left ventricular (LV) hypertrophy, other clinical evidence of the hypertrophic cardiomyopathy (HCM) phenotype was present, including abnormal electrocardiogram with T-wave inversion in leads II and III, aVF, and Q waves in leads V4 to V6 (IV-3), or mild systolic anterior motion of the mitral valve (IV-6). One offspring (IV-11) died of progressive heart failure due to obstructive HCM and was tested retrospectively on a stored DNA sample extracted from peripheral blood obtained prior to death. Although cardiac evaluation was not available in any of the donor's parents, grandparents, or siblings, the donor reported that he was unaware of any evidence of HCM in these family members. The cause of death in the paternal grandmother (I-2) was reported to be a “heart attack” at age 56 years. Both of the donor's parents underwent prosthetic valve replacement. All offspring with unshaded pedigree symbols had reportedly normal cardiac evaluations. Diamond represents 4 additional offspring who did not participate directly in the study but have not pursued genetic testing and have had ongoing cardiac evaluations that were reportedly normal.
  • Implantable Cardioverter-Defibrillators and Prevention of Sudden Cardiac Death in Hypertrophic Cardiomyopathy

    Abstract Full Text
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    JAMA. 2007; 298(4):405-412. doi: 10.1001/jama.298.4.405
  • Hypertrophic Cardiomyopathy, Sudden Death, and Implantable Cardiac Defibrillators: How Low the Bar?

    Abstract Full Text
    JAMA. 2007; 298(4):452-454. doi: 10.1001/jama.298.4.452
  • Hypertrophic Cardiomyopathy: A Systematic Review

    Abstract Full Text
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    JAMA. 2002; 287(10):1308-1320. doi: 10.1001/jama.287.10.1308
  • JAMA May 12, 1999

    Figure 1: Rare Left Ventricular Morphology in Hypertrophic Cardiomyopathy Caused by Specific Genetic Defects

    A, Left ventricular (LV) angiograph in a patient with midcavity obstructive hypertrophic cardiomyopathy (HCM) caused by Met149Val mutation of the essential light chain of myosin. B, Left ventricular angiogram in patient with midcavity obstructive HCM caused by Glu22Lys mutation of the regulatory light chain of myosin. In both cases, massive LV hypertrophy at the level of the papillary muscles has reduced LV chamber size to a narrow tunnel that connects the proximal LV cavity to a distal aneurysm. Atrial and ventricular pacing leads are also evident. C, Left ventricular angiogram in an HCM patient with Leu908Val β-myosin mutation. The midcavity hypertrophy has caused subtotal obstruction, preventing contrast from filling of a distal aneurysm.
  • Advances in Molecular Genetics and Management of Hypertrophic Cardiomyopathy

    Abstract Full Text
    JAMA. 1999; 281(18):1746-1752. doi: 10.1001/jama.281.18.1746
  • JAMA May 12, 1999

    Figure 2: Sarcomere Contractile Proteins

    The sarcomere is made up of contractile proteins organized into thick and thin filaments. The thick filament consists of β-myosin heavy chains (Myosin), essential light chains (ELC), and regulatory light chains (RLC). The thin filament consists of several proteins including actin, tropomyosin (α Tm), troponin C (TnC), troponin I (TnI), and troponin T (TTnT). Myosin has 3 functional domains: a head, a neck, and a tail (or rod). The myosin head contains an adenosine triphosphate–binding pocket (ATP cleft), and an actin binding site. The neck allows extension of the myosin for interaction with actin, and the tail anchors the molecule. Hydrolysis of ATP to adenosin diphosphate and Pi by (ATPase activity of the myosin head) powers translocation of actin by the myosin head. Binding of an ATP to myosin then dissociates myosin from actin. In hypertrophic cardiomyopathy, sarcomeric mutations may affect different stages of this contraction and relaxation process and interfere with the proper functioning of the myosin molecular motor.
  • Clinical Course of Hypertrophic Cardiomyopathy in a Regional United States Cohort

    Abstract Full Text
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    JAMA. 1999; 281(7):650-655. doi: 10.1001/jama.281.7.650
  • JAMA February 17, 1999

    Figure 1: Ages at Death in 277 Patients With HCM

    Deaths due directly to hypertrophic cardiomyopathy (HCM) (n=29) and those unrelated to HCM (n=16) are shown separately. Three patients judged to have HCM-related death had associated atherosclerotic coronary artery disease.
  • JAMA February 17, 1999

    Figure 2: Cumulative Survival After Initial Diagnostic Evaluation Among Patients Diagnosed as Having HCM at 20 Years or Older

    Total mortality (death from any cause) is shown for 234 patients with hypertrophic cardiomyopathy (HCM) compared with that expected in the US general population after adjustment for age, sex, and race. The vertical bars represent 95% confidence intervals for survival probability estimates at selected points. The observed number of deaths was 39, with an expected number of 33 in 1771 patient-years, resulting in observed and expected total annual mortality rates of 2.2% and 1.9%, respectively (P=.17 for a 1-sided test).
  • JAMA February 17, 1999

    Figure 3: Cumulative Survival After Initial Diagnostic Evaluation Among Patients Diagnosed as Having HCM at Younger Than 20 Years

    Total mortality is shown for 43 unselected patients with hypertrophic cardiomyopathy (HCM) compared with that expected in the US general population after adjustment for age, sex, and race. The vertical bars represent 95% confidence intervals for survival probability estimates at selected points (the wide confidence limits are the result of the small sample size). The observed number of deaths was 6, with an expected number of 0.37 in 465 patient years, resulting in observed and expected total annual mortality rates of 1.3% and 0.08%, respectively (P<.001 for a 1-sided test).
  • JAMA February 17, 1999

    Figure 4: Survival According to Clinical Variables

    Probability of survival (by Kaplan-Meier estimates) is shown for 4 clinical variables that were significantly associated with outcome in 277 unselected patients with hypertrophic cardiomyopathy. A, Severity of symptoms at initial diagnosis expressed in terms of New York Heart Association (NYHA) functional class (P=.004). B, Occurrence of atrial fibrillation (paroxysmal or chronic) (P=.002). C, Peak instantaneous left ventricular outflow tract gradient (<30 or ≥30 mm Hg) estimated by Doppler echocardiography; preoperative gradient was used in patients undergoing myotomy-myectomy (P=.01). D, Magnitude of maximum left ventricular wall thickness (≤25 or >25 mm) from 2-dimensional echocardiogram (P<.001).
  • THE MECHANISM OF APOPLEXY

    Abstract Full Text
    JAMA. 1954; 155(6):578-578. doi: 10.1001/jama.1954.03690240044017