ABSTRACTS
TUESDAY, APRIL 27, 1982 AM HYPEWROPH/C CARDlOhlYOPAlWES 10:30- 12:oo ASYMMETRIC SEPTAL HYPERTROPHY: IDENTIFICATION OF PATIENTS WIT" SIGNIFICANT OBSTPIJCTION BY NONINVASIVE METHODS. Harisios Boudoulas, M.D., F.A.C.C.; Dimitrios Mantsouratos, M.D.: Young H. Sohn, M.D.: Richard P. Lewis, M.D., F.A.C.C.; Arnold M. Weissler, M.D., F.A.C.C., Wayne State Univ., Detroit, Ml and Ohio State Univ, Columbus, OH. While asymmetric septal hypertrophy (ASH) can be diagnosed noninvasively, identification of patients (pts) with significant obstruction (ohs) require catheterization. In 49 pts with ASH systolic time intervals (STI), echocardiograms (Echo) and catheterization were performed within 48 Eighteen pts were without ohs, 16 with mild to hours. moderate ohs (gradient l-50 mmHg) and 15 with significant obs (gradient > 50 mmlig). A high degree of correlation was found between corrected left ventricular ejection time (LVETI) and gradient (r = .871. LVETI in pts with ASH but no olx was shorter than norms1 (389 + 17 vs 415 + 10, p < 0.011. All pts with significant ohs had LVETI > 423 msec (2SD above mean for pts with ASH and no ohs) and only (100% 1 pt without significant ohs had LVETI > 423 msec. sensitivity, 97% specificity, 94% positive predictive In 5 pts in predictive value). value and 97% negative whom LVETI and gradient were measured before and during isoproterenol (Iso) infusion changes in both parameters were parallel (r = .75). In an additional pt changes in LVETI and in gradient during serial Iso infusions were parallel and dose related (r = .91). No other echo (including SAM) and ST1 parameters reliably identified pts Thus, in pts with ASH: 1) with significant obstruction. LVETI is shorter than normal if ohs is not present; 2) LVETI can reliably identify pts with significant ohs not only at rest but also during adrenergic stimulation.
"SAW-FISH" MILKING OF THE LEFT ANTERIOR DESCENDING CORONARY ARTERY. AN ANGIOGRAPHIC SIGN OF HYPERTROPHIC CARDIOMYOPATHY. Pedro Brugada, MD; Frits W. Blr, MD, Chris de Zwaan, MD; Denis Rev. MD: Hein J.J. Wellens. MD. FACC. Department Hospital,
of.Cardiology, University-of Maastricht, The Netherlands.
Limburg,
'Iwo dimensional &hocardiograms of 69 cases with hypertrophic cardiomyopathy were studied in order to elucidate the relationship of myocardial hypertrophic patterns to Patterns of septal hyperabnormal Q waves (Q) in ECG. trophy (SH), viewed on the parasternal long axis view, were classified into 3 types; Type 1 with a predominant SH in the basal portion, Type 2 with a diffuse SH and Type 3 The extenwith a predominant SH in the apical portion. sion of hypertrophy to LV and RV was evaluated on the short axis view of LV. The incidences of Q in 25 cases with Type 1 SH (60%) and in 20 cases with Type 2 SH (55%) were significantly higher (P
INFECTIVE ENDOCARDITIS IN HYPERTROPHIC CARDIOMYOPATHY: ANALYSIS OF 5 PATIENTS REQUIRING MITRAL VALVE REPLACEMENT
Annadal
The morphologic aspect at coronary arteriography of systolic compression (SC) of the left anterior descending coronary artery (LAD) was evaluated in 12 patients (pts). 6 Pts had SC of LAD not associated to other cardiovascular and 6 pts had SC of LAD associated with abnormalities, hypertrophic cardiomyopathy (HCM)( 4 obstructive and 2 non-obstructive ). Multiple projections of the coronary arteries were analyzed in each pt. SC of the septal perforator branches (SPB) and other epicardial vessels was also evaluated. Results: In the group of pts without HCM, SC of LAD was smooth along a segment and progressive up to the point of image to the vessel. maximal stenosis, giving a “rat-tail” The degree of SC ranged from 60 to 99%. No pt of this group had SC of the SPB or other epicardial vessels. In the group of pts with HCM, SC of LAD was irregular with indentations in the vessel giving it a “saw-fish” image ( figure ) . The degree of SC ranged from 30 to 100%. Five of the 6 pts had SC of the SPB, and 3 pts had SC of other epicardial vessels as well.
CONCLUSIONS: These results indicate that SC of LAD in HCM differs angiographically from SC of LAD duetoan intramural courseof thevessel.It is nostulatedthat inHCMSCof LADandotber epicardialvessels is duetofibe hypertrophy and disarray in thevicin ity ofthecoronaryarteries andnot dueto anintramuralcourse.
VARIATION OF MYOCARDIAL HYPERTROPHY AND ABNORMAL Q WAVES IN HYPERTROPHIC CARDIOMYOPATHY Hidezo Mori,MD; Satoshi Ogawa,MD; Isao Fujii,MD; Hajime Yamasaki,MD; Hiroe Nakasawa,MD; Shunnosuke Handa,MD; Yoshiro Nakamura,MD,FACC, Keio University, Tokyo, Japan.
Joan C. Kishel, MD, Altagracia 11. Chavez, MD, Barry J . Maron, MD Stephen E. Epstein, MD, FACC, Andrew G. Morrow, MD, ;ACC, and William C. Roberts, MD, FACC, National Heart, Lung and Blood Institute, Bethesda, MD Infective hypertrophic
endocarditis
(IE)
in
patients with
cardiomyopathy (HC) is rare and most such reports have been isolated case studies. We have observed 5 patients with HC who had well documented episodes in the past of active IE which healed. All were males and all underwent mitral valve replacement because of severe mitral regurgitation at ages 12-71 years (mean 49.4). Before the active IE, all 5 had symptoms of cardiac
dysfunction but in each the symptoms were worsened considerably by the infection. Additionally, all 5 patients had precordfal murmurs before the active IE and in each the Intensity of the murmur became All 5 had left ventricular outflow tract louder. obstruction with peak systolic pressure gradients ranging from 45-135 mm Hg (mean 87.8). Examination of the operatively excised mitral valves disclosed each to have evidence of healed IE: ruptured chordae tendineae in all 5, cuspal perforation in 2, marginal i4ndentations in all 5, and focal calcific deposits in . Two patients died early postoperatively; the other 3 have survived 2, 7 and 83 months postoperatively, and each has done well, with postoperative improvements of functional class. Thus, infective endocarditis is a major complication of HC. It usually affects the mitral valve, increases its incompetence, and makes it likely that valve replacement will be necessary.
March 1982
The American Journal of CARDIOLOGY
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