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  • 1
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    Online Resource
    Randomized, Double-Blind Crossover Study to Investigate the Effects of Amlodipine and Isosorbide Mononitrate on the Time Course and Severity of Exercise-Induced Myocardial Stunning
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Circulation Vol. 98, No. 8 ( 1998-08-25), p. 749-756
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 8 ( 1998-08-25), p. 749-756
    Abstract: Background —Myocardial stunning may cause prolonged left ventricular dysfunction after exercise-induced ischemia that can be attenuated by calcium antagonists in animal models. To assess their effects in humans, we performed a randomized, double-blind crossover study comparing the calcium antagonist amlodipine (10 mg once daily) versus isosorbide mononitrate (ISMN, 50 mg once daily) on postexercise stunning. Methods and Results —Twenty-four men with chronic stable angina and normal left ventricular function underwent serial quantitative exercise stress echocardiography after 3 weeks on each treatment to assess the degree of postexercise stunning with simultaneous sestamibi single-photon emission computed tomography perfusion scans at peak stress to quantify the ischemic burden. Exercise time ( P =1), maximum ST depression ( P =0.48), and sestamibi single-photon emission computed tomography scores ( P =0.17) were unchanged between treatments. Stunning occurred more often with ISMN than amlodipine (82% versus 48%). The global and segmental stress echocardiography parameters of stunning were attenuated in patients while taking amlodipine compared with ISMN. Shortening fractions and ejection fractions were less impaired 30 minutes after exercise in patients receiving amlodipine (3.5±1.4% versus 2.5±1.4%, P =0.014, and 59.7±5.4% versus 54.5±8%, P 〈 0.001); similarly, the isovolumic relaxation period was less prolonged with amlodipine (93±15.5 versus 106.3±14.9 ms, P =0.018). Conclusions —Despite comparable levels of ischemia, amlodipine attenuated stunning when compared with ISMN. This beneficial effect may relate to a prevention of the calcium overload implicated in the pathogenesis of stunning.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.98.8.749
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
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  • 2
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    Tachycardia-induced cardiomyopathy caused by atrial flutter responding to DC cardioversion
    Mark Allen Group ; 1999
    In:  Hospital Medicine Vol. 60, No. 4 ( 1999-04), p. 305-306
    Details
    In: Hospital Medicine, Mark Allen Group, Vol. 60, No. 4 ( 1999-04), p. 305-306
    Abstract: A58-year-old man presented in February 1996 to his local hospital with a true posterior myocardial infarction for which he received thrombolysis. He subsequently underwent exercise testing which was terminated because of chest pain and anterior ST depression of 〉 2 mm after 6 minutes of a Naughton Balke protocol. He proceeded to coronary angiography which demonstrated severe triple vessel coronary artery disease. The left ventriculogram demonstrated posterior hypokinesis but overall left ventricular (LV) contractile function was well preserved with an ejection fraction (EF) calculated at 49%. He was in sinus rhythm and had chronic stable angina. In September 1996 he underwent revascularization on prognostic grounds. Five days postoperatively he developed atrial flutter for which he was started on amiodarone 200 mg once daily and subsequently discharged. Two weeks later he was readmitted with progressive dyspnoea and peripheral oedema. He was found to be in clinical heart failure and atrial flutter with a ventricular rate of 150. He subsequently underwent a successful DC cardioversion reverting to sinus rhythm following a single 200J DC shock. He was discharged on amiodarone 200 mg once daily, frusemide 80 mg once daily, enalapril 10 mg once daily and aspirin 75 mg once daily. In November 1996 he presented in atrial flutter with heart failure. An echocardiogram was performed showing a dilated hypokinetic left ventricle with an EF of approximately 20% (Table 1). He was anticoagulated and underwent a further DC cardioversion in February 1997 which successfully reverted him to sinus rhythm. Echocardiography was performed following reversion to sinus rhythm (Table 1) which revealed a dilated LV with global systolic dysfunction and functional mitral regurgitation (EF=30%). In April 1997 he reverted to atrial flutter and had significant effort dyspnoea with an exercise tolerance of 50 yards. He was again successfully cardioverted and commenced on sotalol 80 mg twice daily in an attempt to maintain sinus rhythm. He subsequently remained in sinus rhythm with a marked symptomatic improvement (New York Heart Association Grade 1 dyspnoea and no clinical evidence of cardiac failure). Echocardiography in July 1997 demonstrated a significant improvement in LV dimensions and systolic contractile function (EF=50%) with values equivalent to pre-surgery.
    Type of Medium: Online Resource
    ISSN: 1462-3935 , 2053-4299
    URL: Article
    DOI: 10.12968/hosp.1999.60.4.1773
    Language: English
    Publisher: Mark Allen Group
    Publication Date: 1999
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