SUMMARY Hemodynamic and metabolic studies were performed in 15 patients without heart disease (controls, group A), in 21 patients with typical stress-induced anginal pain but normal coronary and left ventricular angiograms (angina pectoris with normal arteriogram, group B), and in 10 patients with angiographically proved coronary artery disease (CAD, group C). Coronary dilatory capacity, determined by measuring total myocardial blood flow at rest and during maximal coronary vasodilatation (dipyridamole, 0.5 mg/kg i.v.), was markedly reduced in group B and C patients. In group B patients, left ventricular catheter biopsy specimens revealed no evidence of small-vessel disease, but did show histologic alterations of mitochondria. During atrial pacing, the control subjects showed no changes in myocardial lactate uptake, whereas in group B patients, myocardial lactate production occurred. In contrast to controls, patients in group B showed a significant decline in ejection fraction and circumferential fiber shortening during isometric exercise. These findings suggest that myocardial ischemia is the cause of angina pectoris in patients who have angina but normal coronary arteriograms.THE PARADOX of patients suffering from typical stress-induced anginal pain who have normal coronary and left ventricular angiograms has been reported in recent studies.1'~3 The nature of this disease is unknown, and it has been also called syndrome X.5 Myocardial ischemia that is caused by an abnormal affinity of hemoglobin for oxygen, coronary arterial spasm or occlusive disease of small coronary arteries not visualized by coronary arteriography have been suggested as possible causes of this syndrome.4' 6, 14 To evaluate further patients who have angina pectoris but normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) Coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilatation; (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of myocardial cells; (3) myocardial lactate metabolism was studied at rest and during atrial pacing; and (4) left ventricular function was assessed during rest and during exercise.

The pathogenesis of angina pectoris in patients with left ventricular hypertrophy secondary to arterial hypertension and with normal coronary arteries remains uncertain. We measured coronary blood flow (argon method) in 12 control subjects and in 16 patients with arterial hypertension at rest and after intravenous administration of dipyridamole (0.5 mg/kg). In the patients with arterial hypertension, coronary blood flow response to dipyridamole was markedly reduced ( the extravascular component of coronary resistance.5-13 To further evaluate hypertensive patients with angina but with normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilation and (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of the myocardial cells. Materials and methodsGroup A (control subjects) consisted of 12 patients (seven men, five women; mean age 44.8 years) without detectable heart disease. These patients suffered from recurrent atypical chest pain and they were referred for coronary arteriography to exclude an organic cause of the symptoms. All patients in this group had normal electrocardiograms (ECGs) at rest and during exercise and normal coronary and left ventricular angiograms.Group B comprised 16 patients (11 men, five women; mean age 51.4 years) with arterial hypertension class 1 or 11.14 The history of hypertension varied from 4 to more than 20 years (average 9.5 + 6.2 years). Patients were treated in addition to thiazide-type diuretics with /-adrenergic blocking agents (n = 12) and/or hydralazine (n = 3) or prazosin (n = 3). All patients had typical stress-induced angina pectoris that could be promptly relieved by nitroglycerin. The ECG showed evidence of left

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We analyzed data from 68 consecutive patients with congestive cardiomyopathy to evaluate the prognostic significance of quantitative morphologic findings in left ventricular myocardium as compared with the prognostic significance of left ventricular hemodynamics. Left ventricular endomyocardial biopsy specimens were obtained from all patients during diagnostic heart catheterization. Myocardial fiber diameter, volume fraction of interstitial fibrosis, and intracellular volume fraction of myofibrils were determined by light-microscopic morphometry. All patients had normal coronary arteriograms, but reduced left ventricular ejection fractions. There were 23 deaths during a mean follow-up period of 1124 days. Multivariate regression analysis (Cox model) revealed that left ventricular ejection fraction (p < .00001) and left ventricular systolic pressure (p < .01), but not morphometric findings in biopsy specimens, were independent predictors of cardiac death. Thus, morphologic findings in the left ventricular myocardium do not contribute significantly to the prognostic evaluation in patients with congestive cardiomyopathy studied by hemodynamic and angiographic methods. Circulation 70, No. 6, 923-928, 1984. SEVERAL MORPHOLOGIC features of the myocardium in patients with congestive cardiomyopathy have been described. [1][2][3][4][5][6] However, the significance of quantitative morphometric data as independent predictors of survival has not been analyzed.With this study we aimed to determine the prognostic value of quantitative morphologic findings in left ventricular endomyocardial biopsy specimens as compared with that of left ventricular hemodynamic data in patients with congestive cardiomyopathy. MethodsPatients. The study group consisted of 68 consecutive patients (55 men and 13 women) 22 to 62 years old who had congestive cardiomyopathy and were studied invasively between August 1976 and January 1981. Only patients with left ventricular systolic contractile dysfunction entered the study. Patients with coronary artery disease (diameter reduction of a major coronary vessel of ¢25%), a history of systemic hyper-

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Two cases are reported of migrating Kirschner wires, which had been inserted for stabilisation of bony defects of the thoracic cage. The wires migrated in both patients to the heart and caused life threatening complications like pericardial tamponade, arrhythmias and cardiac insufficiency. Indications for removal of foreign bodies from the heart are discussed. Attention is drawn to the fact that the ends of Kirschner wires must be bent in order to prevent migration.

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