Akira Ohyagi

Effect of diltiazem on pacing-induced ischemia in conscious dogs with coronary stenosis: Improvement of postpacing deterioration of ischemic myocardial function

The effects of diltiazem on regional myocardial function were examined in conscious dogs subjected to rapid cardiac pacing during coronary arterial stenosis. Ultrasonic dimension gauges were implanted within the left ventricle for measurement of the control and ischemic segment lengths. During coronary stenosis, percent shortening in the ischemic segment decreased by 18 percent. Heart rate was then suddenly increased by rapid cardiac pacing and this resulted in a further reduction of ischemic segmental shortening. On cessation of pacing, there was early potentiation of rate of increase of left ventricular pressure (dP/dt) and of control segmental shortening with subsequent exponential decay in sequential beats. In the ischemic segment, percent shortening returned to the control level in the first postpacing beat, became severely depressed at 5 seconds after pacing and gradually returned to the control level over the subsequent 5 minutes. Twenty minutes after administration of diltiazem, cardiac pacing was repeated in the same manner and there was less marked potentiation of dP/dt of the first postpacing beat. There ws no significant change in the postpacing dimension and function of the control segment; however, in the ischemic segment, although shortening of the first beat after termination of the pacing was similar, the post stimulation deterioration of shortening was significantly improved, percent shortening being augmented from 7.4 to 10.6 percent at 5 seconds (p less than 0.05). These findings indicate that diltiazem exerts protective effects on the ischemic myocardium by promoting a rapid recovery from ischemia.

Adaptations of the left ventricle to chronic volume overload induced by mitral regurgitation in conscious dogs

SummaryTo assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, end-diastolic (ED) D had increased by 9% from 34.2±2.4 mm (SEM) (P<0.001), wit significant thinning of the wall thickness (from 8.2 to 7.7 mm,P<0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control,P<0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation. Despite a progressive increase in diameter, longitudinal segment length did not increase throughout the study, suggesting that the ventricle assumes a more globular appearance, as an additional compensatory mechanism to prevent excessive enhancement of diastolic wall stress, Initially elevated plasma norepinephrine concentrations (from 127±28 to 256±69 pg/ml,P<0.05) tended to decrease with the development of hypertrophy (202±55 pg/ml). These data support the view that hypertrophy and change in shape of the left ventricle take place during the course of chronic adaptation to volume overload and normalize the elevated wall stress as a negative feedback. Along with the decrease in wall stress, the initially enhanced sympathetic activity decreases gradually during adaptation to chronic volume overload.

Effect of ICI 118,587 on Left Ventricular Function During Graded Treadmill Exercise in Conscious Dogs

Effect of ICI 118,587 (corwin, ICI), a new cardioselective beta-partial agonist, on left ventricular (LV) function was studied and compared with that of isoproterenol and propranolol in 10 conscious normal dogs, instrumented with a micromanometer and pairs of ultrasonic crystals for analysis of LV wall motion. Heart rate, LV dP/dt and mean circumferential shortening velocity were measured at rest and during 3 levels of treadmill exercise (Ex). Before drug administration (control), the heart rate, dP/dt, percent shortening and mean circumferential shortening velocity were enhanced linearly along with the graded Ex. The Ex response curve shifted upward during isoproterenol infusion and downward after the administration of propranolol. With ICI, hemodynamic and contractile indexes were enhanced at rest as with isoproterenol, while these indexes were depressed during maximal Ex as after propranolol. The Ex response curve after ICI crossed the control response curve at a moderate level of Ex. Thus ICI exerts positive inotropic and chronotropic effects at rest when basal sympathetic tone is low, whereas it exerts negative inotropic and chronotropic properties at maximal Ex when sympathetic tone is high. The inherent dual action of this drug is expected to open a new field of treatment for ischemic heart disease with or without heart failure.

A ruptured large aneurysm of the ductus arteriosus.

A 60 year old man was admitted with acute back pain followed by hoarseness. An aneurysm of the ductus arteriosus Botalli was diagnosed and an operation was recommended because of the high risk of complications such as rupture, embolism, or infection. The patient and his family refused surgery, however. The patient died suddenly of a rupture of the aneurysm a year later; necropsy confirmed the diagnosis. Several diagnostic methods were used and enhanced computed tomography gave the best representation of the aneurysm as it was seen at necropsy. This case indicates that enhanced computed tomography is probably the most useful investigation in patients with this type of aneurysm and it confirms the importance of an aneurysmectomy.

Kawasaki disease complicated by acute myocardial infarction 9 years after onset

17. Lindberg HA, Berkson DM, Stamler J, Poindexter A: Totally asymptomatic myocardial infarction: An estimate of its incidence in the living population. Arch Intern Med 5:628, 1960. Melichar F, Jedlicka V, Havlik L: A study of undiagnosed myocardial infarctions. Acta Med Stand 174:761, 1963. Margolis JR, Kannel WB, Feinleib M, Dawber TR, McNamara PM Clinical features of unrecognized myocardial infarction-silent and symptomatic. Eighteen year follow-up: The F ,ammgham study. Am J Cardiol 32:1, 1973. Rosen1 ran RH, Friedman M, Jenkins CD, Straus R, Wurm M, Kositchek R: Clinically unrecognized myocardial infarction in the Western collaborative group study. Am J Cardiol 19:776, 1967. Kannel WB, Abbott RD: Incidence and prognosis of unrecognized myocardial infarction: An update on the Framingham study. N Engl J Med 311:1144, 1984.

Dynamic changes in left ventricular regional wall thickness during premature ventricular contraction in conscious dogs

The contractile pattern of the regional left ventricular wall during premature ventricular contraction was analyzed in conscious dogs instrumented with an ultrasonic dimension gauge across the anterior and posterior left ventricular walls. Aortic flow was measured with an electromagnetic flow probe. A single premature ventricular contraction was induced by stimulating either the anterior or posterior wall with varied coupling intervals from 380 to 650 msec. Stroke volume of premature ventricular contraction was significantly smaller than that of premature atrial contraction with identical coupling intervals. In premature contractions, stroke volume was linearly related to coupling intervals. Though there was no isovolumic wall thickening in premature atrial contraction, the wall started to thicken during isovolumic ventricular systole in premature ventricular contraction. There was a clear inverse correlation between the ratio of the isovolumic wall thickening to the total wall thickening and coupling intervals. In premature ventricular contractions with identical coupling intervals, the deformation of thickening characteristics was more pronounced in regions with closer proximity to the ectopic focus. Thus it is concluded that the pump function is depressed in premature ventricular contraction, in part due to the increased ratio of wall thickening during isovolumic systole before the opening of the aortic valve. Isovolumic wall thickening increases along with the shorter coupling intervals and closer proximity to the ectopic focus. These alterations in left ventricular mechanical function due to ectopic contraction might induce serious sequelae, depending upon the ectopic focus in the presence of already depressed regional function.