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International Journal Elsevier
of Cardiology, 23 (1989) 130-134
Congestive heart failure associated with diabetes mellitus Takehisa Fukuhara, Hideyuki Fujioka and Masahiko Kinoshita Fmt Department of Internal Medicine, Shiga University of Medical Science, Setatsukinowa-rho, Ohtsu 520-21, Japan (Received
4 April 1988; revision
A case of typical congestive heart failure associated with diabetes mellitus is reported. The case was diagnosed on the basis of biopsy findings such as basal laminar thickness and of angiographically normal coronary arteries. The therapy, including insulin, resulted in normalization of electrocardiographic abnormalities and improvement of myocardial contractility. Key words:
Introduction We report here a rare case of typical congestive heart failure associated with diabetes mellitus, but without either coronary sclerosis or renal failure. Case Report A 66-year-old woman who had had diabetes mellitus for 5 years was admitted with dyspnea. She was treated with sulfonylurea, but showed poor diabetic control. Correspondence to: Takehisa Fukuhara, M.D.. First Department of Internal Medicine. Shiga University of Medical Science. Setatsukinowa-cho, Ohtsu 520-21, Japan. 0167-5273/89/$03.50
:Q 1989 Elsevier Science
Serum glutamic oxalacetic transaminase at 17 IU and creatine phosphokinase at 30 IU were at normal levels. Fasting serum glucose concentration was hyperglycemic (from 157 to 449 mg/dl). She had neuropathy and retinopathy, although proteinuria was negative. On the day of admission the patient’s chest roentgenogram (X-P) showed pulmonary congestion and cardiomegaly with cardiothoracic ratio of 71%. Her electrocardiogram already showed ST-T wave abnormalities one month before admission, but still no dyspnea. Her electrocardiogram on admission revealed the same abnormalities (Fig. 1A). Myocardial perfusion scintigraphy using thallium-201 disclosed no perfusion defects in the wall of the left ventricle (Fig. 1B). Angiographically the coronary arteries were completely normal. However, the left ventriculogram revealed hypokinesis and dilatation
Exerg _- ~__ - ____ -d -
Fig. 1A. Serial electrocardiographic recordings. a. Normal electrocardiographic pattern half a year before admission. b. ST-T abnormalities were already evident before the patient complained of dyspnea. c. Admission day: the same abnormalities as in (b). d. Normalization during the clinical course is evident.
Fig. 1B. Myocardial
defects of the left ventricle.
Fig. IC. Clinical
to treatment with digitalis and diuretics, a long-term significant improvement of cardiac impairment.
I1111 IMl I1111 I1111 IIII1I1111Illll I1111I1111IIll1IIlll III11I1111 llll 1111Illi 1111llil Ill1 III1Ill1 Ill1 1111HII 1111
IllI i /111 1; IIII Ill/ IIll IIll1I1111 I_/ Ill1 /!lI~lll~ 1 I1111 IIll1I!IIi LVDd LVDs F,S E,F Fig. 1D. An enlarged
58 mm 52 mm 0.1 28 %
LVDd 50 ITIT ygs ;“,t E:F
left ventricular dimension (LVDd) and a decreased percent fractional shortening (F.S.) were found after admission. Improvements were found during the clinical course. E.F. = ejection fraction.
X 36000 -Basement
Fig. 2. Light and electron micrographic findings. A. Light micrograph shows a scarcity of myofibril in myocytes, but no mononuclear cell infiltration or fibrosis of the interstitial tissue (Hematoxylin and Eosin, X 125). B. Electron micrographs disclose a high glycogen content in the sarcoplasmic, basal laminar thickness. mitochondrial swelling with reduced matrix density and dilated sarcoplasmic reticulum. Staining with uranyl acetate and lead citrate. Left panel: x 9960: right panel: x 29 880.
(end-diastolic volume index: 111 ml/m2, ejection fraction: 32%). Light microscopic studies showed no mononuclear cell infiltration or tissue fibrosis. There was a moderate scarcity of myofibril in the cytoplasm of myocytes, whose diameter ranged from 12 to 20 pm (Fig. 2A). Electron microscopy disclosed an increasing number of glycogen granules, mitochondrial swelling with reduced matrix density, dilated sarcoplasmic reticulum and especially both capillary and myocyte basal laminar thickness (Fig. 2B). Clinical course (Fig. 1C): in addition to basic therapy with diuretics and digoxin, a half-year therapy with insulin and diltiazem resulted in marked cardiac improvement: normalization of ST-T abnormalities (Fig. lA), reduction of the cardiothoracic ratio (from 71 to 48%) and improvement of left ventricular enlargement and contractility (Fig. 1D). Discussion Myocardial damage in diabetics may be due, in addition to atherosclerosis, to pathological [l] and spastic  changes in small coronary arteries, as well as to many and varied metabolic derangements due to insulin deficiency per se . Jackson et al.  described that ultrastructural alterations paralleled a reduction in myocardial contractility. Biopsied myocardial tissues from diabetics have shown a significant increase in the basal laminar thickness of the capillary vessels . These findings are consistent with those shown in our biopsies. Although small coronary artery disease cannot be completely ruled out as a cause, the degree of ischemia was less intense because there were no perfusion defects on the scintigrams nor were there increases in serum creatine phosphokinase and glutamic oxalacetic trans-
aminase levels. Digitalis and diuretics have been recognized as effective in congestive heart failure. although these drugs have failed to normalize systolic function and electrocardiographic abnormalities in patients with dilated cardiomyopathy. Since treatment with some drugs resulted in significant improvement in cardiac abnormalities, it is suggested that congestive heart failure in our case was a specific heart muscle disease associated with diabetes mellitus. In addition to insulin, diltiazem may also cause the microvascular focal constriction described by Factor et al.  to dilate for improvement of myocardial blood perfusion. Finally congestive heart failure associated with diabetes mellitus can be diagnosed on the basis of three factors: (1) therapy including insulin can improve cardiac abnormalities; (2) myocardial biopsy discloses some diabetic changes such as basal laminar thickness: and (3) angiographically the coronary arteries are normal. References Hamby RI, Zoneraich S. Sherman L. Diabetic cardiomyopathy. J Am Med Assoc 1974:229:1749-1754. Factor SM. Bhan R, Minase T, Wolinsky H, Sonnenblick EM. Hypertensive-diabetic cardiomyopathy in the rat. an experimental model of human disease. Am J Path01 1981;102:219-228. Dhalla NS. Pierce GN, Innes IR, Beamish RE. Pathogenesis of cardiac dysfunction in diabetes mellitus. Can J Cardiol 1985;1:263-281. Jackson CV, Mcgrath GM, Tahiliani AG, Vadlamudi RVSV. Mcneill JH. A functional and ultrastructural analysis of experimental diabetic rat myocardium. Diabetes 1985;34: 876-883. Fischer VW, Bamer HB, Leskiw ML. Capillary basal laminar thickness in diabetic human myocardium. Diabetes 1979;28:713-719.