To determine the clinical usefulness of adenosine Tl-201 imaging for the evaluation of coronary artery disease, 22 patients with suspected coronary artery disease who underwent adenosine and exercise Tl-201 single photon emission computed tomography (SPECT) were studied. The peak levels of heart rate (83 vs 123 bpm, p< 0.001), systolic blood pressure (124 vs 164 mmHg, p< 0.001), diastolic blood pressure (70 vs 86 mmHg, p< 0.01) and rate pressure products (10220 vs 20410 bpm × mmHg, p< 0.001) were markedly smaller during adenosine infusion than during exercise. Segmental agreements between adenosine and exercise tests were 90% (218 of 242 segments) regarding the presence of perfusion defects and 89% (215 of 242 segments) regarding the presence of redistribution. Regional Tl-201 defects during adenosine testing were closely correlated with those of exercise testing. Adenosine and exercise tests showed similar sensitivities for the identification of individual coronary stenosis (85% vs 78%). However, in patients who were unable to perform adequate exercise (maximal heart rate < 120 bpm), the sensitivity of adenosine imaging tended to be higher than that of exercise imaging (92% vs 69%, p=0.07) Adenosine Tl-201 imaging is an alternative to the exercise test for assessing the severity and loci of coronary artery disease, especially in patients who are unable to perform adequate physical exercise.

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Specific binding sites for insulin-like growth factor I (IGF-I) and their expression during cardiac myocyte hypertrophy were studied by autoradiographic analysis of right ventricular biopsy specimens from patients with hypertrophic cardiomyopathy (9 cases), dilated cardiomyopathy (8 cases), and sick sinus syndrome (5 cases). Frozen specimens were cut into 5 /μm-thick sections and thaw-mounted on albumin-coated slides. After incubation with [¹²⁵I]IGF-I, with or without excess cold IGF-I, autoradiography was performed, and grains over myocytes were counted microscopically. Binding of [¹²⁵I]IGF-I was inhibited in a dose-dependent manner by unlabeled IGF-I and competed for by IGF-I > IGF-II>insulin. The maximal grain density was higher in hypertrophic cardiomyopathy (186±47/1.8×10^-2 mm²) than in dilated cardiomyopathy (124±13/1.8×10^-2 mm²) or sick sinus syndrome (98±18/1.8×10^-2 mm²) (p<0.01). There was a strong correlation between the maximal grain density and the diameter of right ventricular myocytes in hypertrophic cardiomyopathy (r=0.83), but no similar correlation was observed in dilated cardiomyopathy or sick sinus syndrome. These data suggest that IGF-I receptors are present in adult human cardiac myocytes, and that IGF-I receptors are related to the development of myocyte hypertrophy in hypertrophic cardiomyopathy.

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Blood pressure (BP) and heart rate (HR) (BP waveforms) are affected by external stress during waking and BP is reduced to its lowest level (base BP) during sleep. This study investigated the relationship between BP waveforms while awake and base BP waveforms during sleep. The intra-arterial BPs of 64 inpatients (34 males and 30 females, age: 42±11, mean±SD) with mild essential hypertension were measured for 24 h by the telemetry method. The average 1n (SBP/DBP) (m) while awake and the m at base BP (1n: natural logarithm, SBP' systolic BP, DBP: diastolic BP) had approximately the same values in each patient (mean difference: -0.02±0.07). The product of the RR interval (60/HR) and DBP (RR×DBP) while awake and at base BP had almost the same value (mean difference: -3.2±10 mmHg·sec). According to the Windkessel model, the RR interval during which blood-flow volume in relation to the m value is at its highest can be inferred as S (e^m-1)/(e^m-m-1) (S: systolic time). Using this formula, we developed a formula to estimate base RR from waking m. BP, and RR. Calculations with this estimate formula produced a very slight difference (0.0±0.1 sec) between estimated and actual values for base RR. For the most part, it was possible to infer the base DBP value from the estimated base RR using RR×DBP while awake (mean difference: -3.7±7.0 mmHg). These results suggest that the base BP waveform may be the most efficient pattern, and that waking BP waveforms change based on the base BP waveform during sleep.

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The short- and long-term prognosis for acute myocardial infarction after reperfusion was examined in 175 patients with successful emergency angioplasty and in 29 failed cases. During hospitalization, more cardiac events occurred in the failed group than in the successful group (58.6% versus 12.6%; p<0.001), especially cardiac death and coronary bypass surgery (27.6% versus 4.0%, and 41.4% versus 4.6%; p<0.001, respectively). The only difference found in the incidence of post-discharge cardiac events was a higher frequency of cardiac death in the failed group (9.5% versus 1.2%; p<0.02). The failed group also had a lower cumulative survival rate at 5 years (69.0% versus 95.3%; p<0.01). Cox proportional hazard analysis showed that the results of angioplasty, cardiac index, peak creatine kinase level, and the number of diseased vessels were significant independent variables for the prediction of subsequent cardiac death at long-term follow-up. Thus, successful reperfusion by emergency angioplasty improved the prognosis of acute myocardial infarction, even when other important variables were considered.

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Using an enzyme-linked immunosorbent assay, we measured anti-adenine nucleotide translocator (ANT) antibody in control subjects and in patients with dilated cardiomyopathy (DCM), myocarditis, and other heart diseases. Analysis with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, Western blotting, and immunoabsorption tests confirmed accurate purification of the ANT protein and correct measurememt of anti-ANT auto-antibody. Anti-ANT anti-body was detected in 6 of 37 cases (16%) of DCM and in 5 of 12 cases (42%) of myocarditis. This antibody was not positive in other heart diseases or in apparently healthy controls. There were no differences between anti-ANT autoanti-body-positive and -negative DCM or myocarditis patients in any of the cardiac parameters examined (left ventricular ejection fraction, LVEF; left ventricular end-diastolic dimension, LVDd; and cardiothoracic ratio, CTR). Moreover, in patients who were positive for anti-ANT auto-antibody, no positive correlations were found between the parameters and anti-ANT antibody titers in either DCM or myocarditis. Although these results indicate that the detection of anti-ANT antibody was achieved at a high specificity and could have certain diagnostic value in DCM and myocarditis, there was no statistically significant relationship between the cardiac parameters (LVEF, LVDd, and CTR) and anti-ANT antibody titers in either DCM or myocarditis. Some compensatory mechanism of ventricular function may mask the effects of the anti-ANT auto-antibody or alternatively, this auto-antibody may have mimic effects on the pathogenesis and/or progression of DCM and myocarditis.

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The role of nitric oxide in the coronary vasodilation caused by acetylcholine or bradykinin in perfused guinea-pig hearts was investigated by using 1 mM L-N^G-nitro arginine (L-NNA), a specific inhibitor of the formation of nitric oxide from L-arginine. L-NNA increased coronary perfusion pressure and inhibited the vasodilator responses to acetylcholine and bradykinin. The extent of vasodilation was evaluated in terms of the reduction of perfusion pressure from the initial baseline that had been induced by U-46619. L-NNA markedly attenuated coronary vasodilation caused by 5×10^-11 mol of acetylcholine from 15±1 to 4±1 mmHg (p<0.01), and that caused by l×l0^-11 mol bradykinin from 21±2 to 8±1 mmHg (p<0.01). On the other hand. L-NNA only weakly inhibited coronary vasodilation caused by 5×10^-7mol of acetylcholine from 40±3 to 27±4 mmHg (p<0.01), and that caused by 1×10^-9 mol of bradykinin (from 39±2 to 32±2 mmHg (p<0.01). L-NNA had no effect on the vasodilation induced by 1 × 10^-8 mol of bradykinin. Ibuprofen, cyclooxygenase inhibi-tor, did not affect these vasodilatory responses. These results suggest that the formation of nitric oxide from L-arginine in coronary resistance vessels helps to regulate vascular tone, and that prostaglandins are not related to the vasodilatory responses to acetylcholine or bradykinin. Thus, nitric oxide is largely responsible for the vasodilatory responses to low doses of acetylcholine or bradykinin. However, mechanisms other than the release of nitric oxide or prostaglandins may be involved in the vasodilatory responses to high doses of acetylcholine or bradykinin.

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The role of changes in preload in maintaining stable hemodynamics during coronary obstruction was assessed in the presence of myocardial ischemia due to occlusions of the left anterior descending (LAD) and left circumflex (LCX) coronary arteries. Changes in preload (mean left atrial pressure) to maintain a constant stroke volume after coronary occlusion were examined in 18 anesthetized dogs (LAD occlusion in 9 dogs, LCX occlusion in 9 dogs). The level of ischemia was assessed sonomicrometrically. Ventricular function curves relating left atrial pressure to stroke volume were assessed during a control state and after I min of coronary occlusion. The extent of preload reserve after coronary occlusion was examined on the ventricular function curves and was defined as the change in mean left atrial pressure required to maintain stroke volume at the level of the control state under conditions of regional ischemia. Ischemic size was determined by a stereo-angiogram after the animals were sacrificed. The extent of preload reserve (X) was linearly related to the ischemic size (Y) in both LAD (Y=0.90+0.16X, r=0.76, p<0.001)and LCX (Y=-1.79+ 0.19X, r=0.79, p<0.001) occlusions. The slopes of the regression lines in LAD and LCX occlusions were the same. The X intercepts of these lines were -5.6% and 9.4% of the left ventricular weight in LAD and LCX ischemia (p<0.001), respectively. Thus, the presence of systolic wall motion abnormalities due to coronary occlusion can be compensated for hemodynamically by changes in the preload reserve. This process appears to be more sensitive in cases of LAD occlusion than in cases of LCX occlusion.

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Objectives: Protons produced during ischemia may increase intracellular Na⁺ (Na⁺i) through Na⁺/H+ exchange, and may lead to Ca²⁺ overload through Na⁺/Ca²⁺ exchange to cause myocardial stunning. This study investigated whether an increase in the H⁺ buffering capacity of the perfusate or a reduction of H⁺ production by a brief hypoxic preperfusion before ischemia would reduce myocardial stunning. We also investigated whether the protective effect of these maneuvers depends on the free [Ca²⁺] of the perfusate. Methods: Isolated rat hearts were preperfused with oxygenated or hypoxic buffer (pH 7.4) containing 100 mM of either sucrose or HEPES for 10 min, followed by 15 min of total ischemia and 30 min of reperfusion. To investigate the dependence of the effects of HEPES or a brief hypoxic preperfusion, the free Ca²⁺ concentration in the buffer was changed from 1.25 mM to 2.5 mM in some hearts. Results: Oxygenated preperfusion with buffer containing HEPES and 1.25 or 2.5 mM Ca²⁺ improved the metabolic and functional recovery with a decrease in the accumulation of Na⁺ i during ischemia and in ⁴⁵Ca²⁺ uptake during re-perfusion. A brief hypoxic preperfusion with 1.25 mM Ca²⁺ provided a similar protective effect whereas no protective effect was observed when the [Ca²⁺] was raised to 2.5 mM. Conclusions: An increase in the H+ buffering capacity or a brief hypoxic pre-perfusion reduced myocardial stunning with improved metabolic recovery, and reduced Ca²⁺ uptake. However, the effects of these interventions were affected differently by the free [Ca²⁺] of the perfusate, which suggests that they work, at least in part, through some different mechanism(s).

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Rupture of a chronic postinfarction aneurysm of the left ventricle is rare and usually fatal. A 63-year-old man with rupture of a true left ventricular aneurysm 67 days after myocardial infarction was treated successfully with resection of the aneurysm. The postoperative course was uneventful.

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