The characteristics ECG findings as they relate to myocardial changes during long-term course of hypertrophic cardiomyopathy (HCM) were studied. Serial changes in ECG were compared with changes left ventriculogram and bi-ventriculogram in 15 patients with HCM without intraventricular conduction disturbance. Serial changes in ECG findings, with special reference to the negative T wave, were categorized in three group; 1) 5 patients with increase or appearance of the negative T wave (A-1 group). 2) 4 patients with decrease or disappearance of the negative T wave (A-2 group). 2) 6 patients without significant changes in the T wave (B-group). A-1 group presented a marked increase in SV₁+RV₅, and of the thickness of anterior and apical wall, and a decrease of the peak dV/dt/EDV (end diastolic volume-normalized peak filling rate), serially. End diastolic volume (EDV) and ejection fraction (EF) did not change significantly. The configuration of left ventriculogram changed from a round form to a spade-like form. A-2 group presented a marked decrease in SV₁+RV₅, the thickness of anterior and apical wall, peak dV/dt/EDV and peak dV/dt/V (left ventricular volume of the time of peak filling-normalized peak filling rote). EF decreased serially, 2 cases of A-2 group presented the clinical picture of dilated cardiomyopathy in the end stage. In B group, SV₂+RV₅, the wall thickness and left ventricular function did not change, serially. In conclusion, serial observations of ECG are useful for assessing alterations in wall thickness, LV-form and LV-function.

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To investigate the influence of wall hypertrophy and myocardial lesions on the regional contractile dynamics of the left ventricle (LV) in patients of hypertrophic cardiomyopathy (HCM), we obtained the thicknesses of the ventricular septum (VS) and posterior wall at end-diastole and systole (E.Td, E.Ts) from echocardiograms made before death for 11 patients of HCM and 6 patients of secondary concentric hypertrophic heart disease (SHH), and the percent regional systolic wall thickening normalized by that of 15 normal controls (%NRWT). We then compared the %NRWT with the pathological wall thickness (P. T.), myocyte diameter (MD), and percent areas of fibrosis (%F) and disarray (%D) in specimens of the corresponding portion from each autopsied heart. The %NRWT in the VS of HCM patients was significantly less than that in SHH patients. All of the MD, %F and %D in the LV wall of HCM patients were significantly greater than those in SHH patients. The %NRWT in the LV wall of HCM patients and SHH patients correlated inversely with the E.Td (r=-0.53, p<0.02 and r=-0.70, p<0.02. respectively), but not with the E.Ts or P.T. The %NRWT in the LV wall of HCM patients had an inverse correlation with the %F (r=-0.59, p<0.005). Furthermore, that in the VS had an inverse relationship with the %D (r=-0.63, p<0.05). Thus, it is suggested that not only LV hypertrophy, but also LV myocardial lesions affect the abnormality of the regional LV contractile dynamics in HCM patients. In addition, observation of the regional contractile dynamics by echocardiography may be useful for speculating on myocardial lesions associated with this disease.

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The indications for revascularization surgery and its effect on myocardial regions showing persistent defects in thallium myocardial images are controversial. The effects of aortocoronary bypass surgery on myocardial perfusion and wall motion in the regions with persistent defects were evaluated in 47 patients with thallium-201 single photon emission computed tomography and left ventriculography. In areas showing persistent thallium defects preoperatively the rate of improvement of perfusion was only 24% by postoperative thallium imaging, and 57% by wall motion analysis. These results were significantly inferior to those of regions with transient defects, which were 84% and 82%, respectively. A persistent defect may not be a definitive marker of a non-viable scar, but the results of surgery on such regions were unsatisfactory. It is concluded, therefore-that revascuralization surgery in regions with persistent defects is not always recommended and that the indications for surgery should be individually determined with operative risk balanced against benefits.

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This investigation deals with a statistical probatory that patients with primary (PH) or secondary (SH) hypertension may be correctly diagnosed by a discriminant analysis of the chronobiologic characteristics computed on the 24-hour blood pressure (BP) patterns. The methodology concerning non-invasive 24-h BP monitoring, chronobiologic analysis and the discrimination process is detailed. Substantial dissimilarities were found in the statistical distribution for systolic and diastolic BP rhythmometric parameters (mesor, amplitude and acrophase) by a retrospective assessment of two groups, consisting of 54 patients with PH and 16 patients with SH. The group-related distribution for rhythmometric parameters was found to be significantly different to generate a statistically significant intergroup discriminatory boundary. The discriminant analysis correctly diagnosed patients with PH and SH in a percentage of about 91% and 63%, respectively. The high incidence of success is convincing that the combination of 24-h BP monitoring/ chronobiologic analysis/ discrimination process can be a practical tool for confidently selecting patients with a presumable PH or SH.

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The aim of our studies was to examine if the baroreceptor reflex induced by intravenous injection of nitroglycerin (NG) nearly nullifies the vasodilator action of NG on the systemic capacitance vessels in dogs anesthetized with pentobarbital. We performed total spinal anesthesia (TSA) in open-chest dogs to eliminate the baroreceptor reflex. Dogs in which mean blood pressure (MBP) was maintained at about 100 mmHg by continuous intravenous infusion of epinephrine formed the TSA 100 group, and those in which MBP was maintained at about 70 mmHg formed the TSA 70 group. Dose-response curves relating 56 different doses (0.8 to 200μg/kg) of intravenous NG, to changes in mean circulatory pressure (%ΔMCP) and to changes in total peripheral resistance (%ΔTPR), were constructed. These data were compared with those from untreated dogs. In addition, we also studied plasma catecholamine (CA) concentrations before and after the intravenous injection of NG. (1) There was no significant difference in the dose-response curves of NG for %ΔTPR between the 3 groups. (2) There was no significant difference in the dose-response curves for %ΔMCP between the 2 TSA groups. However, there was significant difference in the dose-response curves for %ΔMCP between the TSA groups and the untreated dogs. The dose-response curves for %ΔMCP in the TSA groups shifted upwards as compared with that of the untreated dogs. (3) In the TSA 100 group, there was no significant increase in the plasma CA concentrations with 100μg/kg of NG. In the untreated group, intravenous injection of 12.5μg/kg and 100μg/kg of NG caused a dose-related fall in MBP and a dose-related rise in the plasma norepinephrine and epinephrine concentrations. Our results suggest that the vasodilator action of NG on the systemic capacitance vessels in the untreated dogs was counterbalanced partly by the vasoconstriction produced by the baroreceptor reflex, with its direct vasodilator effect masked when the hypotensive doses of NG were given acutely.

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A 67-year-old man developed an acute myocardial infarction shortly after normal exercise testing. His clinical history and findings from emergency coronary arteriography suggested that coronary artery spasm followed by intraluminal thrombosis might have been responsible for the myocardial infarction. Although intracoronary thrombolysis two hours after the onset of chest pain provided continued patency of an occluded vessel, serial myocardial perfusion scintigraphies documented myocardial injury, which was probably induced by reperfusion, rather than myocardial salvage.

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Prevalence of silent myocardial ischemia in exercise test was retrospectively reviewed from 749 tests performed for 513 patients with definite evidence of ischemic heart disease. The clinical significance was studied and absence of transient ischemia, occurrence of transient ischemia with and without pain were observed in 48%, 30% and 22% of the tests, respectively. Anginal pain was frequently observed in exercise tests for patients with severe coronary artery disease and low exercise tolerance. A large number of tests showing ischemic response were discontinued due to symptoms other than anginal pain and hence silent myocardial ischemia could be thought to be a result of ischemic state which does not reach the angina threshold. Silent myocardial ischemia was frequently observed during usual daily life. However, a definite correlation between severity of transient ischemia and presence or absence of chest pain in the same individuals was not obtained from the study. A day to day variation in the angina threshold might be responsible. In general, silent myocardial ischemia was not rare. However, the consistent condition was very unusual. In angina of effort (EA) and old myocardial infarction (OMI), 3.7% and 12.3% were silent, respectively. A higher incidence was obtained in OMI than in EA. This is important for the management of these patients. The mechanism of silent myocardial ischemia and the cause of the different incidence of this state between EA and OMI were not defined and remained to be further studied.

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The purpose of this study was to investigate the frequency and characteristics of silent myocardial ischemia in patients with proven ischemic heart disease using ambulatory ECG monitoring, and to clarify possible mechanisms for the absence of symptoms during these attacks. A total of 182 patients, including 78 patients with stable effort angina (EA), 12 with unstable angina (UA), and 92 with prior myocardial infarction (MI), were examined. During daily activities, 43% and 56% of all transient ST-segment depression observed was asymptomatic in patients with EA and MI, respectively. In addition, 74% of all ischemic episodes were asymptomatic in patients with UA. In patients with EA, 35% exhibited both symptomatic and asymptomatic attacks, and the duration and magnitude of ST-segment depression were greater for symptomatic attacks than for asymptomatic attacks. On the other hand, in patients with MI, 55% had only asymptomatic attacks. When asymptomatic episodes in patients who had only asymptomatic attacks were compared with symptomatic episodes in patients who had only symptomatic attacks, asymptomatic episodes tended to be associated with a greater magnitude of ST depression. They were also significantly longer in duration than the symptomatic episodes. All patients with UA had both symptomatic and asymptomatic episodes, and the magnitude and duration were significantly greater during the former. These results lead us to conclude that: (1) silent myocardial ischemia is observed frequently in patients with EA and MI during daily activities. In particular, patients with MI tend to have more severe silent ischemia. (2) In patients with EA and UA, the severity of ischemia is a fundamental factor in determining the presence or absence of pain during an ischemic attack. (3) In patients with MI, the occurrence of silent myocardial ischemia probably depends upon alteration in the pain threshold or perception.

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To clarify the clinical and prognostic significance of silent myocardial ischemia (SMI) after acute myocardial infarction (MI), the clinical characteristics and long-term prognosis after discharge in 525 medically treated survivors after acute MI were investigated. According to the presence of post-infarction angina and results of all exercise tests during hospitalization, 309 patients without ischemic episodes were classified into control group, 59 patients with SMI into SMI group and 157 patients with post-infarction angina into AP group. Previous MI (29%, 24%, 11%, respectively), non-Q wave MI (34%, 34%, 15%) and multivessel disease (69%, 61%, 33%) were more frequent in the SMI and AP groups than in the control group. These indicated clinical characteristics in patients with SMI were similar to those in patients with angina pectoris. The incidence of angina prior to MI onset in patients with SMI was lower than in patients with post-infarction angina. This may suggest that there is some common mechanism keeping them silent in the pre- and post-MI period. During the mean follow-up period of 5.5 years, 93 patients died and 78 had a recurrent MI. Cumulative total and cardiac mortality, and incidence of recurrent MI by actuarial method were higher in the SMI as well as AP group than in the control group. There was no statistically significant difference in prognosis between SMI and AP group. We conclude total ischemic burden, not only symptomatic but SMI, should be treated using currently available therapeutic modalities for further improvement of long-term prognosis in survivors after acute MI.

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The diagnosis of silent myocardial ischemia in the aged remains controversial. In this study to evaluate the basic state of silent ischemia in the aged, a total of 972 consecutive autopsy cases (mean 79.0 yrs of age) were analyzed in terms of coronary atherosclerotic diseases. The following results were obtained: (1) Severe coronary occlusive lesions simultaneously detected in the three major coronary arterial branches were found in 85 cases (8, 7%), of which may correspond to one representation of silent ischemia. (2) There were 218 cases of MI (22.4%), of which 106 (49%) were never documented to have MI during life. The latter may correspond to unrecognized MI. It was considered to be caused by 1) small or middle-sized MI in 66 cases and 2) lateral or nontransmural MI in 29 out of 40 large MI cases (more than 4.9 cm in diameter). (3) 30 cases (54%) out of 56 fresh and large MI with a correct diagnosis revealed no chest pain. This is an incidence of painless MI in the aged. This painless group showed a significant difference in the incidence of a correct diagnosis of MI (51% vs 89%), combined arrhythmia (47% vs 79%) and the association of CVD (47% vs 11%) compared with chest pain group.

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1. Objectively, provoked angina is different from non-provoked angina. a) During pacing stress testing, provoked angina showed lesser increase in coronary sinus blood flow. b) During Ergotamine testing, variant angina showed a more marked decrease in flow. c) The myocardial lactate extraction ratio was lower during the pacing induced angina. 2. During the asymptomatic period, the polyparametric changes which would become manifest appeared following differing intervals. The early recognition of the myocardial ischemia was achieved by detection of the abnormality of the regional cardiac wall motion using a newly developed device, the cardiomoveogram. 3. Therefore, we can at least conclude that silent myocardial ischemia is not a good prognostic sign.

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TO investigate myocardial perfusion in silent myocardial ischemia, we performed exercise stress myocardial tomography with thallium-201 (T1) in 85 patients with coronary artery disease (CAD). Exercise stress myocardial tomography was obtained both immediately after exercise and three hours later. Patients were classified into two groups according to the presence (Symptomatic Group, n=36) or absence (Silent Group, n=49) of chest pain during exercise stress. Clinical features (age, gender and history of myocardial infarction) and arteriographically determined severity of CAD were the same in both groups. The extent of myocardial ischemia (% Ischemia) estimated by exercise stress myocardial tomography was the same in each group (30±10% in Silent Group, 28±12% in Symptomatic Group, NS). The severity of exercise-induced myocardial ischemia was expressed as a minimal value of myocardial T1 washout rate (minimal WOR) of each patient. Although exercise heart rate was identical in both groups, minimal WOR in Silent Group was significantly higher than that of Symptomatic Group (4±10% vs -16±14%, p<0.001). the study in patients who exhibited both silent and symptomatic ischemia showed same results. These findings suggest that the severity of ischemia is a fundamental factor in determining the presence or absence of pain during exercise induced ischemia.

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To evaluate myocardial blood flow and glucose utilization, N-13 ammonia and F-18 deoxyglucose positron emission tomography were performed in 33 patients with myocardial infarction. The N-13 ammonia study was performed at rest and during supine exercise, and the F-18 deoxyglucose was done at rest after≥5 hours of fasting. Based on angina, exercise-induced hypoperfusion, and deoxyglucose uptake, 3 groups of patients were classified; 10 patients in group I (neither angina nor exercise induced hypoperfusion), 8 patients in group II (painless exercise-induced hypoperfusion) and 15 patients in group III ( anginal patients with/without exercise-induced hypoperfusion). The F-18 deoxyglucose positron study demonstrated accumulation of deoxyglucose in 6 patients in group I, 7 in group II, and 14 in group III. Thus, our result indicated that a significant number of patients with antecedent myocardial infarction had exercise-induced hypoperfusion and/or altered glucose metabolism without accompanying anginal pain.

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The present study was canued out to clarify the relationship between silent myocardial ischemia in patients with angina pectoris and onset of myocardial infarction, and the former's prognostic significance. The peak incidences of onset of myocardial infarction in patients were at 2 a.m., 9 a.m., 2 p.m., 8 p.m., and 9 p.m., and the peak onsets of transient silent myocardial ischemia in angina pectoris patients were at 9 a.m., 2 p.m., 8 p.m., and 9 p.m. Thus the most likely onset times were almost the same with both events. Of 169 patients with coronary artery disease admitted for treatment, 128 patients had no anginal attacks during follow-up and the remaining 41 had persistent angina despite adequate medical treatment. Holter monitoring electro-cardiography was performed twice with the non-angina patients, during admission. Of these 128 patients, 54 showed no silent myocardial ischemia on either of the electrocardiographic recordings, 34 showed silent ischemia with the first Holter monitoring but not with the second one, and the remaining 41 showed silent myocardial ischemia on both tests. The subsequent incidences of " cardiac events" were 9.4%, 14.7% and 36.6%, respectively for these three groups. Therefore, it is concluded that the presence of silent myocardial ischemia is closely related to onset of myocardial infarction and is an important prognostic factor in patients with coronary artery disease.

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Twenty-four hour ambulatory electrocardiographic recording was performed in 56 patients with variant angina admitted to the coronary care unit in order to evaluate the incidence and pathophysiology of silent episodes of ST elevation. Of 696 episodes of ST elevation of more than 0.1 mV identified during a recording period of 141 days, 531 (76%) episodes were completely silent. The incidence of silent episodes increased as the number of total ischemic episodes per day increased. Silent ST elevation revealed a significantly shorter duration and a lower intensity than symptomatic ST elevation. However, there were wide overlaps in the duration and intensity of ST elevation between silent and symptomatic episodes. In some patients, silent and symptomatic episodes of similar duration and intensity were observed. Arrhythmias during ischemic episodes such as premature ventricular contractions, ventricular tachycardia, high grade atrioventricular block, and sinus arrest were observed in 32 of 56 patients, 57% of cases and 9% of the total episodes. Arrhythmias were more common during symptomatic episodes (29%) than during silent ones (9%, p<0.01), but serious arrhythmias such as ventricular tachycardia, high grade atrioventricular block and sinus arrest occurred even during silent episodes. In both silent and symptomatic episodes, the duration and intensity of ST elevation were significantly lower in ischemic episodes with arrhythmias than in those without arrhythmias. These results suggest that 1) the majority of ischemic events are silent in patients with variant angina; 2) the severity of ischemia seems to be an important factor as the cause of anginal pain, but additional factors may be involved; 3) arrhythmias were more common during symptomatic than silent episodes.

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We have assessed the sequential changes in left ventricular function and ECG in 39 patients with coronary artery disease (CAD) using an ambulatory ventricular function monitor. Following radionuclide ventriculography, the instrument detectors were place over the region of the left ventricle and lung, and beat-to-beat left ventricular time activity curve and modified V5 ECG data were continuously monitored for up to 6 hours (mean 2.5 hours(, while the patient performed various daily activities. Thirty-six episodes of transient ejection fraction (EF) decrease (6-18%) were recorded in 16 patients, 12 were symptomatic and 24 asymptomatic. ST segment changes were recorded in 6 of the 12 symptomatic episodes, EF began to drop 30 to 90 seconds before the onset of the symptoms. Of 14 episodes of significant ST segment depression in five patients, 11 were associated with a significant EF decrease. We conclude that the combination of left ventricular function and ECG monitoring is a promising means for determining incidence of silent and symptomatic ischemia and for severity of ischemia in patients with CAD.

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Bradykinin, alone or in combination with prostaglandin, is thought to produce pain in patients with coronary heart disease. To elucidate this further, we have investigated and compared serum bradykinin, TXB₂ and 6KPGF_1α levels in patients with silent myocardial ischemia (SMI, n=18), painful myocardial ischemia (PMI, n=8) and normal subjects (NL, n=18). In addition, SMI and PMI subjects were given exercise testing and the results then compared. After Holter monitoring for 48 hours, exercise testing was performed. Blood was sampled in the morning between the Holter and exercise regimen. Maximal heart rate, systolic blood pressure and the double products were not significantly different between the SMI and PMI groups. The duration of exercise for the SMI group was 7.08±2.1 min vs 5.9±1.9 in the PMI group (p<0.10). Plasma bradykinin was 14±3 pg/ml in the SMI group and 15±3 in the PMI group (N.S), whereas it was 7±4 in the NL (p<0.05). The TXB₂/6KPGF_1α for the SMI group was 1.3±0.3, which was significantly higher than that for the NL group (0.8±0.3, p<0.01), though this did not greatly differ from the PMI group (1.2±0.3). These results suggest that SMI patients under Holter monitoring who manifest no symptoms but show significant ST segment depressions must receive the same careful attention given to PMI patients. In both group of patients bradykinin and prostaglandin metabolism is similarly change, as was demonstrated by exercise stress testing.

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