Search

Background and Purpose: Administration of adenosine attenuates myocardial stunning after reperfusion in a canine experimental ischemic model. However, it is unknown whether administration of adenosine triphosphate disodium (ATP) during reperfusion can attenuate myocardial stunning after coronary recanalization in patients with acute myocardial infarction (MI). Therefore, we sought to elucidate the effects of ATP administration on serial changes of left ventricular systolic function before and after coronary recanalization., Methods: In 27 patients with first ST-elevation acute anterior MI, in whom primary percutaneous coronary intervention (PCI) was completed within 10 h after symptom onset, ATP at a mean rate of 103 microg/kg/min (n=16) or normal saline (n=11) was intravenously administered for 1 h during reperfusion. Left ventricular regional wall motion within the initially severely ischemic region was serially analyzed using the standard wall motion score index (WMSI) by transthoracic echocardiography., Results: Means of WMSIs were similar shortly before primary PCI in both groups (2.79 in ATP group and 2.69 in controls). They changed to 2.56 and 2.22 shortly after PCI, 2.49 and 2.39 on day 2, 2.34 and 2.30 on day 3, 2.19 and 2.25 on day 10, and 1.85 and 2.02, 6 months later, respectively. Transient improved regional wall motion within the initially severely ischemic region was observed shortly after PCI in controls (10.3% of observed segments); however, it was significantly suppressed in the ATP group (2.55%). The percent recovery of WMSI on day 10, which was defined as WMSI on day 10 normalized by improvement of WMSI for 6 months, was 63.8% in ATP group and 65.7% in controls, implying ATP administration could not reduce myocardial stunning by day 10 after primary PCI., Conclusions: The high-dose administration of ATP during primary PCI prevented transient improved wall motion shortly after coronary recanalization rather than preventing left ventricular stunning. These results suggest that ATP can prevent reperfusion injury during primary PCI.

Loss of the vasodilator response to acetylcholine (Ach), an endothelium-dependent vasodilator, has been demonstrated in animal models of atherosclerosis and in atherosclerotic coronary arteries of humans studied in vitro. The response of normal coronary arteries on angiograms to the intracoronary injection of Ach in patients with familial hypercholesterolemia (FH) was studied. Ten patients with FH (mean age, 53.6 +/- 6.5 years) with a mean serum total cholesterol of 334.8 mg/dl and 12 controls (mean age, 55.8 +/- 14.5 years) with a total cholesterol level of 183.6 mg/dl, and with normal coronary arteries on angiograms were studied. Patients with clinical histories suggestive of coronary spastic angina were excluded from this study. A bolus of 20, 50 micrograms Ach and 2 mg isosorbide dinitrate (ISDN) were infused into the left coronary artery in each subject. Changes in coronary diameters were measured after each injection with a videodensitometric analysis system. In the control group, the diameter at the middle segments of the left anterior descending artery (LAD) and at the proximal and middle segments of the left circumflex artery (LCX) increased significantly in response to Ach; whereas, in the FH group the diameter at the proximal segments of the LAD decreased significantly. There were significant differences in the coronary diameter changes in response to 50 micrograms Ach at the proximal and middle segments of the LAD and the LCX between the 2 groups. In contrast, between these 2 groups, there were no significant differences in the vasodilator responses to ISDN, a direct vascular smooth muscle dilator. The vasodilator response of coronary artery to Ach was diminished in patients with FH.

The functional significance of the coronary collateral circulation remains controversial. It has been suggested that collateral circulation possibly helps prevent myocardial ischemia. Seventeen target lesions in 15 patients were studied to determine the relationship between the extent of the coronary collateral circulation and the degree of ventricular dysfunction during percutaneous transluminal coronary angioplasty (PTCA). During the first balloon inflation, diastolic indices such as left ventricular end-diastolic pressure, max negative dP/dt and the time constant of early relaxation were measured immediately before and at 60 sec following balloon inflation. During the second inflation, the contralateral and ipsilateral collateral circulations were evaluated. The latter was graded as follows: 0 = none; I = filling of side branches only; II = partial filling of the epicardial segment; and III = complete filling of the epicardial segment. Following balloon inflation, a significant increase was noted in the time constant of early relaxation in patients with grade 0 collateral circulation (40 +/- 7 to 47 +/- 7 msec: p < 0.01) and grade II collateral circulation (52 +/- 12 to 56 +/- 13 msec: p < 0.05). The percent increase in the time constant of early relaxation of patients with grade 0 and I collateral circulations exceeded that of patients with grade II (p < 0.05) or grade III collateral circulation (p < 0.05). Left ventricular end-diastolic pressure was elevated in all groups during PTCA. There was no significant difference in the percent increase of left ventricular end-diastolic pressure (LVEDP) between the 4 groups. However, LVEDP before PTCA was higher in patients with grade III collateral circulation than in patients in the other groups. Max negative dP/dt did not change significantly in any group. In conclusion, collateral circulation helps prevent myocardial ischemia during acute coronary occlusion, which is most precisely shown by the time constant of early relaxation. The degree of this protective function of collateral circulation seems to vary.

The characteristic of myocardial damage in hypertrophic cardiomyopathy (HCM) was evaluated as to whether the damage is limited to the hypertrophied wall or extends throughout the entire wall. The myocardial damage was detected by exercise thallium-201 (Tl-201) scintigraphy and was evaluated using circumferential profile analysis, calculation of initial uptake and washout rate. Eleven patients with asymmetrical hypertrophy (ASH), whose septal and posterior wall thickness ratio exceeded 1.3 on left ventriculography and biventriculography, and 13 age-matched control subjects without heart disease were studied. The mean values of initial uptake in both groups did not differ significantly, but the washout rate for the entire heart was significantly decreased only in the HCM group (p < 0.05). All of the regional washout rates (antero-septal, apical and postero-lateral) were significantly decreased in the HCM group (p < 0.05), without any difference between the hypertrophied wall and the non-thickened free wall being noted. These results demonstrated that the analysis of myocardial damage by exercise Tl-201 scintigraphy using calculation of the washout rate is a very sensitive means of detecting myocardial damage in HCM, and that such myocardial damage is not restricted to the hypertrophied wall, but rather extends to the entire wall, including the free wall which is not thickened.

In patients with hypertrophic cardiomyopathy (HCM) and essential hypertension (HT), left ventricular dysfunction in early diastole which is associated with left atrial contraction plays an important role in left ventricular filling. To evaluate left atrial booster pump function, we analyzed left atrial preload (left atrial pressure at the end of diastasis; LAPd, left atrial volume index at the end of diastasis; LAVd), left atrial afterload (left ventricular end-diastolic pressure; LVEDP, left ventricular chamber stiffness constant; K), and left atrial ejection indices (left atrial ejection fraction during atrial contraction; LAEF, left atrial ejection volume index during atrial contraction; ACVI). The study subjects consisted of control subjects (n = 5), HT patients (n = 6), and HCM patients (n = 11). The left ventricular wall was significantly thicker in the HT and HCM groups. The left ventricular rapid filling volume index was less in the HT group, and significantly less in the HCM than in the control group. LAPd and LAVd were greater in the HT group than in the control group, and greater in the HCM group than in the HT group. LVEDP and K were greater in the HT group than in the control group, and significantly greater in the HCM group than in the other 2 groups. ACVI was greater in the HT group than in the control group, but in the HCM group, ACVI was significantly less than in the HT group and did not differ significantly from that in the control group. LAEF was significantly less in the HCM group than in the other 2 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The relation of left ventricular diastolic function and the histopathological findings of the myocardium in patients with diabetes mellitus were observed using echocardiography and endomyocardial biopsy. The subjects consisted of six diabetic patients (mean age 49.3 years) and eight normal control subjects (mean age 44.8 years). Coronary angiography had no significant stenotic lesions in their coronary arteries. Their diabetic complications were mild to moderate in severity. Echoes from the left ventricular margin of the septum and from the posterior left ventricular wall were traced on a digitizing board; then the isovolumic relaxation period, rapid filling period, slow filling period and atrial contraction period were determined to calculate fractional shortening (FS), isovolumic relaxation time (IRT), and three filling volumes (RFV, SFV and ACV). The quotients of the left ventricular filling volume and stroke volume were also determined. Right ventricular endomyocardial biopsies were performed to determine the diameters of myocytes, the percentage of fibrosis and the eccentricity e, as a parameter of the degree of myocardial dysarrangement. The results were as follows: IRT was significantly longer and RFV/SV was significantly greater in patients with diabetes mellitus than those among the controls. Also the diameters of myocytes and the percentage of fibrosis were significantly greater, while the eccentricity e was less compared to that of the controls. There were no significant correlations, among IRT, RFV/SV, the diameters of myocytes, and eccentricity e, but the percentage of fibrosis significantly correlated with IRT and RFV/SV (r = 0.62, r = -0.63). IRT and RFV/SV were mainly responsible for the percentage of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

In this study, we investigated correlations of left ventricular hypertrophy and its histopathology with diastolic dysfunction in patients with hypertrophic cardiomyopathy. Nine control subjects and 14 hypertrophic cardiomyopathy (HCM) patients with asymmetrical septal hypertrophy were evaluated. M-mode echocardiography was used to assess fractional shortening (FS), isovolumic relaxation time (IRT), and the left ventricular filling volume index during rapid and slow filling periods and atrial contraction period (RFVI, SFVI and ACVI). End-diastolic thickness of the interventricular septum and posterior wall was determined using biventriculography. Right ventricular endomyocardial biopsies were performed to calculate the diameters of myocytes, the percentage of fibrosis and the eccentricity e which indicates the degree of myocardial disarrangement including disorganization. The FS was normal in the two groups. The IRT of the HCM group was significantly greater and the RFVI significantly less than those of the controls. The left ventricular wall thickness, the diameters of myocytes and the percentage of fibrosis in the HCM group were significantly greater; and the eccentricity e was significantly less, suggesting that myocardial disarrangement was significantly more severe than that in the controls. Significant positive correlations were observed between the IRT and the wall thickness (r = 0.647), between the diameter of myocytes (r = 0.681) and the percentage of fibrosis (r = 0.628), and there was a significantly negative correlation between the IRT and the eccentricity e (r = -0.759). There was a significantly negative correlation between the RFVI and the wall thickness (r = -0.663); and a significantly positive correlation between the RFVI and the eccentricity e (r = 0.579). Multiple regression analyses showed that the diameter of myocytes, the percentage of fibrosis and the eccentricity e all correlated significantly with the IRT (R = 0.821) and the RFVI (R =0.604). The standard regression coefficients of the diameter of myocytes, the percentage of fibrosis and the eccentricity e were 0.253, 0.278 and -0.431 in respect to IRT, and those of the percentage of fibrosis and the eccentricity e were -0.204 and 0.469 in respect to RFVI, respectively. These results indicated that diastolic dysfunction in hypertrophic cardiomyopathy is related not only to the degree of left ventricular hypertrophy, but also to the degree of myocardial hypertrophy, increased interstitial fibrosis, and especially to myocardial disarrangement including disorganization.

The present study was performed to clinically clarify the pathogenesis of hypertensive cardiac hypertrophy (HT) and hypertrophic cardiomyopathy (HCM). Exercise thallium-201 (Tl-201) myocardial scintigraphy using a bicycle ergometer was performed for controls, HT and HCM. The scintigrams were evaluated by the circumferential profile analysis. Furthermore, the changes in Tl-201 dynamics in exercise Tl-201 scintigraphy with verapamil injections were examined in these three groups. Analysis of exercise Tl-201 scintigraphy without verapamil injections showed that the initial uptake did not differ among the three groups, but the washout rate three hours after the Tl-201 injections (WR3) did differ among the three groups. Although the WR3 of HT did not differ from that of the controls, the WR3 of HCM was lower than that of the controls. The WR3 with and without verapamil were compared. Although the WR with verapamil injections equalled that without verapamil injections in the controls and HT, the WR3 with verapamil injections decreased more than did that without verapamil injections in HCM. As an index of great and rapid changes in circulation, the washout rate one hour after the Tl-201 injection (WR1) was calculated. The WR1 without verapamil did not differ among the three groups and did not differ from that with verapamil injections in each group. These results suggest that Tl-201 dynamics of HT differ from those of HCM and lowering of the WR3 in HCM may not be caused by disturbance in the microcirculation, but rather by disturbance of Tl-clearance through the cell membrane and its cytoplasm.

Twenty cases of left ventricular diverticula were gleaned from 4,300 consecutive angiocardiographic records (13 males and seven females whose age ranged from 17 to 78 years with a mean of 52 +/- 16 years). Their findings were compared with those of 16 patients with left ventricular aneurysms due to myocardial infarction. In only one patient was a diverticulum first detected by two-dimensional echocardiography before left ventriculography was performed. None of the patient had an associated midline thoracoabdominal defect. Five patients had premature ventricular beats, two of whom had ventricular tachycardia. Three patients complicated mitral valve prolapse and three atrial septal defect. Of the 20 patients, four each had two diverticula, as opposed to 16 others who each had a single diverticulum. The diameter of the diverticula ranged from eight to 70 mm. The sites of 14 diverticula were along the inferior wall; five in the anterior wall; four in the apex. Morphologically 15 diverticula were bulky outpouchings, six were tongue-like, and three hammocking. All diverticula exceeding 15 mm in diameter and originated near the mitral ring could always be detected in the short-axis view of two-dimensional echocardiography. However, those originating in the apex or of a tongue-like configuration could rarely by detected. Comparative two-dimensional echocardiographic analyses of 16 diverticula, 16 left ventricular aneurysms, and 16 normal left ventricular walls disclosed that the left ventricular aneurysmal wall had a higher echo intensity, but the diverticula had the same wall echo intensity as the normal left ventricular wall. Left ventricular end-diastolic wall thickness in an aneurysm (7.6 +/- 1.5 mm) was lower (p less than 0.01) than the normal left ventricular wall (11.1 +/- 1.3 mm), but it did not differ from the normal left ventricular wall in any case of diverticulum (10.2 +/- 1.5 mm). The percent wall thickening ratio in aneurysms (-3.6 +/- 10.7%) was lower (p less than 0.01) than the normal left ventricular wall (39.8 +/- 10.9%), but it did not differ from the normal left ventricular wall in diverticula (45.8 +/- 16.6%). Regional fractional shortening in the diverticula (41.3 +/- 9.2%) did not differ from that in the normal left ventricular wall (34.5 +/- 5.2%). In conclusion, a small diverticulum without a midline thoracoabdominal defect is not rare, and two-dimensional echocardiography is the diagnostic method of choice in many cases based on the echo features described above.

Electrocardiographic follow-up was conducted for 17 patients with hypertrophic cardiomyopathy including six cases who received left ventriculographic follow-up. 1. Serial ECG changes were as follows: 1) In seven patients negativity of the T wave appeared or increased concomitantly with increased voltage of SV1 + RV5 (A-1 group). 2) In four patients, negativity of the T wave decreased or disappeared with the decreased voltage of SV1 + RV5 (A-2 group). 3) In six patients, there were insignificant changes of both T wave and SV1 + RV5 (B group). 2. Results of serial left ventriculography and biventriculography were as follows: 1) Two patients (A-1 group) showed an increased voltage of SV1 + RV5 (25 mm----48 mm, 42 mm----54 mm), and increased thickness of the apical wall (10 mm----12 mm, 8 mm----11 mm) and the anterior wall (13 mm----16 mm, 10 mm----16 mm). However, the thickness of the posterior and interventricular septal walls did not change. The configuration of the end-diastolic left ventriculogram (RAO 30 degrees) changed from a round configuration to the so-called "beak" configuration. 2) Two patients (A-2 group) showed a decreased voltage of SV1 + RV5 (81 mm----26 mm, 73 mm----53 mm), decreased thickness of the apical wall (18 mm----10 mm, 21 mm----15 mm) and the anterior wall (12 mm----9 mm, 17 mm----12 mm). The end-diastolic left ventriculogram changed from a spade-like configuration to a round configuration. In the analysis of diastolic function measured by digitized cineangiograms using a picture-analyzer, diastolic dysfunction was already present at the initial observation. The diastolic and systolic dysfunction progressed during serial observations. These patients showed the clinical pictures of dilated cardiomyopathy at the final observation. 3) Two patients with no remarkable changes of the T wave (B group) showed insignificant changes in configuration of the left ventriculogram and wall thickness. In conclusion, serial changes in configuration of the left ventricle and wall thickness, especially of the anterior and apical walls, are compatible with the serial changes of the ECG in hypertrophic cardiomyopathy. The patients whose negative T waves decreased or disappeared had diastolic dysfunction at the initial observation, and deterioration of both diastolic and systolic dysfunctions during serial observations.

Fifteen patients, 12 males and three females, with hypertrophic cardiomyopathy (HCM) including three of obstructive type (HOCM) were investigated to observe the long-term course of HCM. Left ventriculography and bi-ventriculography were performed twice serially in all cases. We studied the correlations between the serial ECG changes, especially the negative T wave, and the left ventricular configuration, wall thickness, and left ventricular function. Serial ECG changes included: 1) negativity of the T wave which developed or increased concomitantly with increased voltages of SV1 + RV5 (A-1 group: five cases), 2) the negativity decreased or resolved with decreased voltages of SV1 + RV5 (A-2 group: four cases), and 3) insignificant changes of both T waves and SV1 + RV5 (B group: six cases). In the right oblique views at end-diastole, the configuration of the left ventricle was classified in three forms; (1) spade form (S), (2) round form (R), and (3) intermediate form (SR). The results were as follows: 1. The A-1 group showed increased thickness of the apical and anterior walls, but the thickness of the posterior wall and interventricular septal wall did not change serially. In three cases, the thickness of the interventricular septum showed mild hypertrophy at the initial and final observations. The configuration changed from the R or SR form to the S form. Diastolic dysfunction (peak dV/dt/V, peak dV/dt/EDV) was progressive, but end-diastolic volume and ejection fraction did not change. 2. The A-2 group showed the significantly decreased thickness of the apical and anterior walls. The thicknesses of the posterior wall and interventricular septal wall tended to decrease in all cases. In three cases (75%), the interventricular septal wall was markedly hypertrophied on the initial observation. The configuration changed from the S or SR form to the R form. Left ventricular diastolic function and ejection fraction decreased significantly and end-diastolic volume increased. Two cases showed clinical pictures of dilated cardiomyopathy at the final observation. 3. In the B group, there were no marked changes in wall thickness, left ventricular configuration, or systolic and diastolic functions. In conclusion, serial changes in left ventricular configuration, wall thickness, especially of the anterior and apical walls, and left ventricular function were all compatible with the serial changes of the ECG in hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 400 WORDS)

This study elucidated diastolic left ventricular dysfunction and whether myocardial interstitial fibrosis correlates with diastolic dysfunction in mild to moderate systemic hypertension (HT). Six normotensive subjects, 18 hypertensive patients without left ventricular hypertrophy (LVH) and 10 hypertensive patients with significant LVH were evaluated. M-mode echocardiography was used to determine fractional shortening (FS), isovolumic relaxation time (IRT), and left ventricular filling volume during rapid and slow filling periods and the atrial contraction period (RFV, SFV, ACV). The quotients of the left ventricular filling volume and the end-diastolic volume and stroke volume were also calculated. Simultaneous biventriculography was used to determine the end-diastolic thickness of the interventricular septum and posterior wall. Right ventricular endomyocardial biopsies were performed to calculate the percentages of fibrosis. The FS was normal in all groups. The percentages of fibrosis in the two HT groups were significantly greater than those in the normals. The IRT of the HT groups was significantly greater, and the RFV, RFV/EDV and RFV/SV were significantly less than those of the normals. Multiple regression analysis showed that the wall thickness and the percentages of fibrosis correlated significantly with IRT, RFV, RFV/EDV and RFV/SV. The standard coefficients of correlation of wall thickness and the percentages of fibrosis were 0.333 and 0.239 in respect to IRT, and -0.304 and -0.473 in respect to RFV. There were significant correlations between the percentages of fibrosis and RFV (r = -0.675), RFV/EDV (r = -0.664) and RFV/SV (r = -0.602) in the normals and in cases of HT without LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Two cases of hypertrophic cardiomyopathy (HCM), in whom giant negative T waves resolved during 10 years, are reported. Case 1: A 33-year-old man was admitted in 1975 for careful evaluation because of an ECG abnormality. The ECG revealed a giant negative T wave (GNT) in V5 (-15 mm) and high voltage (SV1 + RV5 = 81 mm). The thickness of the apical wall was 18 mm; the anterior wall, 12 mm; the posterior wall, 16 mm; and the interventricular septum, 17 mm on the left ventriculogram and biventriculogram. The coronary angiogram was normal. From these data, this patient was diagnosed as having HCM. However, follow-up studies disclosed resolution of the GNT with decreased high voltage (SV1 + RV5 = 26 mm). The catheterization performed in 1985 showed a decrease of wall thickness: the apical wall to 10 mm; the anterior wall, 9 mm; the posterior wall, 14 mm; and the interventricular septum, 14 mm. Ejection fraction was markedly decreased from 79.8% to 27.1%, and the wall motion was generally reduced. The coronary angiogram was normal. These findings resemble the clinical pictures of dilated cardiomyopathy (DCM). Case 2: A 58-year-old man was admitted in 1974 because of easy fatiguability. His ECG revealed a GNT in V4 (-10 mm) and high voltage (SV1 + RV5 = 75 mm). The patient was diagnosed as having HCM by cardiac catheterization, right ventricular biopsy and other procedures. In 1985, the depth of the GNT and the voltage of SV1 + RV5 regressed significantly (SV1 + RV5 = 26 mm). The thickness of the apical wall was, 12 mm; the anterior wall, 19 mm; the posterior wall, 13 mm; and the interventricular septum 14 mm during recatheterization. Coronary angiography disclosed stenoses of the left main trunk (75%), the left anterior descending artery (99%) and the left circumflex artery (50%). The right coronary artery was totally occluded. In conclusion, these two cases of HCM had similar changes in their ECG during long-term follow-up studies, but the process was different. One case finally showed clinical pictures of DCM; the other, severe coronary stenoses. These suggested that blood flow to the myocardium is an important determinant for the development of clinical features simulating DCM in cases with HCM.