Assessment of left ventricular myocardial perfusion and diastolic function during acetylcholine-induced diffuse coronary vasoconstriction by Doppler echocardiography and thallium-201 scintigraphy.

BACKGROUND: We investigated whether diffuse coronary vasoconstriction induced by acetylcholine caused myocardial ischemia. METHODS: We studied 30 patients (40 coronary arteries) with spontaneous chest pain or equivocal studies on treadmill exercise testing and no significant coronary stenosis or previous myocardial infarction. During the acetylcholine provocation test, Doppler echocardiography was performed, and thallium-201 was injected intravenously for scintigraphy. We used Doppler echocardiography to measure the ratio of early-to-late peak mitral flow (E:A ratio). RESULTS: When acetylcholine was injected, the coronary arteries showed three different responses. Diffuse coronary vasoconstriction without chest pain or ischemic changes on the ECG was induced in 18 (45%) arteries and the E:A ratio decreased from 0.83 +/- 0.13 to 0.77 +/- 0.13 (P = 0.031). In 17 vessels (control arteries), the E:A ratio did not change significantly (from 0.88 +/- 0.15 to 0.88 +/- 0.18; P = 0.95). In five arteries, focal spasm was induced and the E:A ratio decreased from 0.83 +/- 0.18 to 0.66 +/- 0.13 (P = 0.043). Transient defects on thallium-201 scintigraphy were observed in the territory of eight (80%) arteries with diffuse vasoconstriction and in one (20%) control artery (P = 0.047). CONCLUSIONS: Diffuse coronary vasoconstriction induced by intracoronary acetylcholine can decrease the regional myocardial blood flow (as shown by thallium-201 scintigraphy) and can cause global left ventricular diastolic dysfunction (as shown by the results of Doppler echocardiography).

[Serial change of 123I-BMIPP SPECT imaging during recovery from stunned myocardium after acute myocardial infarction--correlation with 201Tl and two-dimensional echocardiography].

Using 123I-beta-methyl iodophenyl pentadecanoic acid (123I-BMIPP), we investigated changes in myocardial fatty acid metabolism at recovery from stunned myocardium after acute myocardial infarction (AMI), correlation with recovery of regional wall motion and thallium-201 (201Tl) distribution in particular. The subjects were 15 patients who underwent successful reperfusion therapy after the first onset of AMI. None of the patients had multi-vessel disease or ischemic episode during their clinical course. Patients underwent 123I-BMIPP scintigraphy, 201Tl scintigraphy and two-dimensional echocardiography during the acute and chronic phases. Then, we compared regional wall motion with distribution of 123I-BMIPP and 201Tl. Regional wall motion and SPECT were evaluated by the established 16 segment model. In patients, showing serial improvement in regional wall motion, there was 80.0% (8/10) showed normal 201Tl distribution during the acute phase or normalized during the chronic phase. However, distribution of 123I-BMIPP normalized only in 10.0% (1/10) of this group. In examination of each segment that showed serial improvement in regional wall motion, 92.3% (24/26) of these segments showed normal distribution of 201Tl during the acute phase or normalized distribution during chronic phase, despite distribution of 123I-BMIPP improved in only 3.8% (1/26) of these segments. These indicate that, in the process of recovery from myocardial stunning after AMI, abnormal distribution of 123I-BMIPP continued longer than abnormal distribution of 201Tl.

Is ST segment re-elevation associated with reperfusion an indicator of marked myocardial damage after thrombolysis?

OBJECTIVES: The significance of ST segment re-elevation at reperfusion by thrombolysis was evaluated. BACKGROUND: The significance of ST re-elevation has not been studied. Hence, we evaluated whether ST re-elevation is an indicator of marked myocardial necrosis after reperfusion. METHODS: Twelve-lead electrocardiograms were recorded serially, before thrombolysis and immediately after each coronary angiographic procedure during thrombolysis. RESULTS: In 32 patients with acute myocardial infarction, 15 showed transient ST re-elevation at reperfusion (group 1) and 17 showed reduction (group 2). Peak creatine kinase (CK) and CK-MB isoenzyme activity levels were significantly higher in group 1 than in group 2. Twelve patients in group 1 had strongly positive findings on early technetium-99m pyrophosphate scintigraphy, compared with one patient in group 2 (p < 0.001). The regional ejection fraction did not increase from the acute phase to the chronic phase in group 1. The ST deviation before thrombolysis was significantly greater in group 1 than in group 2 (p < 0.001). All 14 patients in group 1 showed Thrombolysis in Myocardial Infarction (TIMI) grade 0 flow and 12 of these patients did not have good collateral flow before thrombolysis. CONCLUSIONS: These data suggest that 1) ST re-elevation at reperfusion is a sign of limited myocardial salvage by thrombolysis, and 2) high ST elevation and TIMI grade 0 flow without good collateral flow before thrombolysis may be predictive variables for marked myocardial necrosis after reperfusion.

Hemodynamic efficacy of E-1020 in comparison with dopamine on acute mitral regurgitation in anesthetized dogs.

To evaluate the effects of a new phosphodiesterase inhibitor, E-1020 (1, 2-dihydro-6-methyl-2-oxo-5-(imidazo [1, 2-a] pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate), on cardiovascular hemodynamics in acute heart failure, we compared its effects with those of dopamine on experimentally produced acute mitral regurgitation in dogs. After the production of mitral regurgitation by transmyocardial chordal sectioning and obtaining a stable state, dopamine (5 micrograms/kg/min) was infused until the peak positive dP/dt (peak (+) dP/dt) increased to about 50% of the predopamine value. After complete recovery, E-1020 (30 micrograms/kg) was infused over 5 min and the data were obtained 10 min later. Both drugs equally increased peak (+) dP/dt, decreased systemic vascular resistance, and increased cardiac output. Left ventricular (LV) end-diastolic pressure, LV end-diastolic segment length (EDL), and mean left atrial (LA) pressure decreased with both drugs. The changes in EDL and mean LA pressure were larger with E-1020 than with dopamine (p less than .01 and p less than .05). Although mean inferior vena caval blood flow volume (mIVCF) increased and mean inferior vena caval pressure decreased with both drugs, the increment of mIVCF was smaller with E-1020 (p less than .001). Thus, E-1020 had not only a positive inotropic effect but also a vasodilatory action both on resistance vessels and on capacitance vessels.

Left ventricular regional wall stress in dilated cardiomyopathy.

Left ventriculography with simultaneous pressure micromanometry was performed in 11 normal control subjects and 17 patients with dilated cardiomyopathy (DCM). Left ventricular silhouettes in the right anterior oblique projection were divided into eight areas, and regional wall stress was computed by Janz's method in each area excluding the two most basal areas. Wall stress was higher in DCM patients than in control subjects (p less than 0.01). The percent area changes from end diastole to end systole in each area were lower in DCM patients than in control subjects (mean for six areas, 22 +/- 14% versus 54 +/- 9%, respectively, p less than 0.01), but the coefficient of variation for the percent area changes in the six areas of the left ventricle in DCM patients was greater than that in control subjects (32 +/- 17% versus 15 +/- 4%, respectively, p less than 0.01), indicating regional differences in hypokinesis. There was a significant negative correlation between end-systolic regional wall stress and percent area change (r = -0.60 to -0.86, p less than 0.05) in each area. Thus, excessive regional afterload may play an important role in causing regional hypokinesis in DCM.

[Venous flow velocity patterns and cardiac function studied by Doppler echocardiography].

To study the relations of central venous flow velocity (VFV) to cardiac pump function, hepatic venous flow velocity was recorded using Doppler echocardiography in six normal subjects and 47 patients with heart disease, of whom 28 had sinus rhythm and 19, atrial fibrillation. The area under the VFV profile during systole and diastole in a cardiac cycle was computed, and termed the VIs (systolic time-velocity integral) and VId (diastolic time-velocity integral), respectively. VIs was divided by the sum of VIs and VId [VIs/(VIs + VId)], and this was termed the VI ratio. The cardiac index (CI) was estimated by Doppler echocardiography. In normal subjects, the VFV pattern in a cardiac cycle was biphasic, the systolic VFV being dominant. In patients with atrial fibrillation, the systolic VFV was attenuated or absent, the diastolic VFV being dominant. The CI correlated well with the VI ratio (r = 0.80; p less than .001) in 14 patients with atrial fibrillation except for five patients with tricuspid regurgitation. Four patients in whom atrial fibrillation converted spontaneously to sinus rhythm showed an increase in the CI and the VI ratio according to the CI-VI ratio relationship. In patients with sinus rhythm, the CI tended to decrease as the VI ratio increased. In 15 patients who had a VI ratio of over 0.75, the CI correlated inversely with the VI ratio (r = -0.70; p less than 0.01). Three of four patients who had the VI ratio of 1.0 died of congestive heart failure. Although there was positive correlation between the CI and VI ratio in patients without effective atrial contraction, there was inverse correlation in patients with effective atrial contraction. It is suggested that the VI ratio could be a good indicator of cardiac pump function.