title: Protection of the hypertrophied myocardium by crystalloid cardioplegia.
abstract: Patients with left ventricular hypertrophy (LVH) have a worse outcome after cardiac surgery than those without hypertrophy. We studied protection of hearts with LVH in an isolated rat heart model using multidose, cold, oxygenated cardioplegia. LVH was produced by banding the abdominal aorta in young rats. Six weeks after banding, this produced a 31% increase in the left ventricular dry weight/body weight ratio compared to two age-matched control groups comprising sham-operated and nonoperated animals. The recovery of cardiac output after arrest was higher in LVH (82 +/- 4% of prearrest) than in sham-operated (69 +/- 4%) or nonoperated (66 +/- 3%) control groups. The improved functional recovery in LVH occurred although there were no differences among the groups in myocardial adenosine triphosphate (ATP) and phosphocreatine (PCr) prior to arrest, at the end of arrest, or after reperfusion. Glycogen levels were also similar among the three groups prior to arrest and after reperfusion but were highest in LVH after arrest. Myocardial oxygen consumption (MVO2) and efficiency, expressed as cardiac output/MVO2, were similar among the groups prior to arrest. Myocardial efficiency after reperfusion declined in all groups but was best preserved in LVH. We also compared the sensitivity of hypertrophied and control hearts to the deleterious effects of calcium in cardioplegia. Calcium in the cardioplegia increased myocardial lactate production during arrest in a dose-related fashion and depressed myocardial levels of ATP, PCr, and glycogen at end arrest in all groups. Cardiac output recovery was also depressed by calcium but was still best in LVH. We conclude that the hypertrophied myocardium is well protected by standard cardioplegia and that calcium in cardioplegia does not preferentially depress recovery in LVH.
authors.affiliation: Department of Surgery, Massachusetts General Hospital, Boston.
authors.forename: N A
authors.initials: NA
authors.lastname: Munfakh
authors.forename: J B
authors.initials: JB
authors.lastname: Steinberg
authors.forename: J S
authors.initials: JS
authors.lastname: Titus
authors.forename: A G
authors.initials: AG
authors.lastname: Denenberg
authors.forename: D D
authors.initials: DD
authors.lastname: O'Keefe
authors.forename: W M
authors.initials: WM
authors.lastname: Daggett
authors.forename: G A
authors.initials: GA
authors.lastname: Geffin
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D003402:Creatine Kinase / Q000378:metabolism; D000077324:Crystalloid Solutions; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D066298:In Vitro Techniques; D007552:Isotonic Solutions; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D010101:Oxygen Consumption; D010710:Phosphates / Q000378:metabolism; D010952:Plasma Substitutes; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000077324:Crystalloid Solutions; D007552:Isotonic Solutions; D007773:Lactates; D010710:Phosphates; D010952:Plasma Substitutes; D019344:Lactic Acid; D003402:Creatine Kinase