Intracoronary nisoldipine: Effects on acute myocardial ischemia during coronary angioplasty

Summary The effects on ischemic myocardium of 0.05 mg nisoldipine given by intracoronary injection were studied in 22 patients subjected to percutaneous transluminal coronary angioplasty. The angioplasty balloon was inflated for periods of 60 seconds. During the occlusion period, pulmonary wedge pressure was measured, an intracoronary epicardial ECG recorded, and ventricular volumes and ejection fraction were determined by means of digital subtraction angiography. After the intracoronary administration of nisoldipine, the onset of the rise in diastolic filling pressure was slightly delayed from 29 to 36 seconds. While affecting neither the rise in filling pressure nor the increase in end-diastolic and endsystolic volumes after 60 seconds of ischemia, nisoldipine delayed the occurrence (from 13 to 33 seconds; p<0.005) and reduced the extent (from 1.5 to 0.6 mV; p<0.001) of ischemic ST elevation in the intracoronary ECG. After nisoldipine, anginal symptoms were clearly reduced during the ischemic phase in the majority of patients. These findings suggest that intracoronary pretreatment with nisoldipine leads to a regional protection of ischemic myocardium without any appreciable effect on ischemia-induced myocardial dysfunction.     

Usefulness of severity of myocardial ischemia on exercise testing in predicting the severity of myocardial ischemia during daily activities

To determine the relation between myocardial ischemic indexes on exercise testing and on ambulatory Holter recording, 60 patients with stable coronary artery disease who exhibited an ischemic response to both testing procedures were studied. All patients performed a Bruce protocol exercise test and underwent 24-hour Holter recording within 2 weeks without antianginal medications. Mean exercise duration was 7.4 +/- 2.8 minutes, mean heart rate at 1-mm ST depression was 118 +/- 20 beats/min and mean maximal ST depression during exercise was 2.2 +/- 1 mm. During Holter recording the average number of ischemic episodes was 4.7 +/- 2.6 per patient, mean duration of daily ischemia was 62 +/- 54 minutes, mean maximal ST depression was 3.2 +/- 1.3 mm and average heart rate at 1-mm ST depression was 93 +/- 17 beats/min. Overall, the correlations between ischemic indexes on both testing procedures were very weak (mean r2 = 0.054). The only exercise variable that had a significant correlation (p less than 0.05) with all Holter variables was heart rate at 1-mm ST depression, yet it correlated very weakly (0.064 less than or equal to r2 less than or equal to 0.125) with most Holter covariates and had a better correlation (r2 = 0.256) only with average heart rate at 1-mm ST depression during Holter. Thus, ischemic indexes on exercise testing cannot accurately predict ischemic indexes on ambulatory Holter recording in patients with stable coronary artery disease who exhibit ischemic changes on both tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Silent myocardial ischemia during daily activities in asymptomatic men with positive exercise test responses

The usefulness of prolonged ambulatory electrocardiographic monitoring (AEM) for detecting ischemia was investigated in 17 asymptomatic men who had ischemic-type ST-segment depression (greater than or equal to 2.0 mm) during treadmill exercise testing. No patient took anti-ischemic medications and all patients underwent coronary angiography. A total of 1,154 hours (range 64 to 72 hours/patient) of high-quality AEM recordings was obtained. Silent ischemia (episodes of asymptomatic ischemic-type ST depression of 60 seconds or longer) occurred in 11 patients during daily activity detected by AEM. In 6 other patients, no myocardial ischemic episodes were found. But 1 of these patients withdrew after only 24 hours of AEM and the remaining 5 had no significant coronary artery disease (CAD). All 11 patients who had silent ischemia had significant CAD (at least 50% stenosis) on angiography. There was wide intrapatient variability in the frequency of silent ischemic episodes. Silent ischemia was identified in 6 of these 11 patients after 24 hours of AEM, in 2 after 48 hours and in 3 after 72 hours. Thus, asymptomatic men with positive exercise test responses and CAD have silent ischemic episodes during daily activity. AEM may be useful in helping to predict which patients with asymptomatic positive exercise test responses have CAD; however, extended AEM periods are required.     

Cardioprotective actions of nisoldipine in postreperfusion myocardial ischemia

Nisoldipine, a dihydropyridine with calcium channel-blocking activity, was studied in myocardial ischemia and reperfusion in cats. At an infusion rate of 3 micrograms/kg/hr, nisoldipine did not significantly alter the product of mean arterial blood pressure and heart rate, the pressure-rate index. When infusion of nisoldipine was started 30 minutes after occlusion and continued for 5 1/2 hours, nisoldipine exerted a marked antiischemic effect. This effect was manifested as a significant reduction in necrotic myocardial tissue expressed either as a percentage of area at risk (p less than 0.01) or as a percentage of total left ventricle (p less than 0.01). The washout of creatine kinase into the circulation was also reduced in nisoldipine-treated cats. When nisoldipine infusion started at 60 minutes after ischemia, the effects were still significant (p less than 0.05) but less striking, and when nisoldipine infusion was delayed until 90 minutes after ischemia, no significant cardioprotection was observed. Nisoldipine also blunted the washout of creatine kinase into the peripheral circulation on reperfusion. Thus nisoldipine exerts a cardioprotective effect in cats during myocardial ischemia independent of reducing myocardial oxygen demand. The effect is optimal when nisoldipine is given during the first 30 minutes of ischemia and declines thereafter, reaching insignificant effects at 90 minutes.     

Characteristics of silent and symptomatic myocardial ischemia during daily activities

In 191 patients with proven coronary artery disease, 24-hour Holter monitoring detected 587 transient episodes of ST depression during daily activities. Of that total, 424 episodes were silent (72.3%) and 163 were symptomatic (27.7%). There were no statistically significant differences between silent and symptomatic episodes as to their mean duration (15.1 vs 14.3 minutes, respectively), heart rate at onset of ST depression (93 vs 96 beats/min, respectively), heart rate at the time of maximal ST depression (114 beats/min, both) and mean maximal ST depression (1.9 vs 2.0 mm, respectively). Of the 191 patients, 104 (55%) had only silent episodes, 33 (17%) only symptomatic episodes and 54 (28%) had both types ("mixed"). All patients, regardless of episode type, were of similar age, received comparable medical therapy, had a similar extent of angiographically documented coronary artery disease and similar episode characteristics. However, mixed-episode patients had significantly more ischemic episodes per day (4.8) than silent-episode (2.6) and symptomatic-episode (1.9) patients (p less than 0.001 for both) and a longer total period of daily ischemia (60 minutes), than the other 2 groups (36 and 28 minutes, respectively, p less than 0.001 for both). Of the 191 patients, 97 (51%) had had a previous myocardial infarction. The characteristics of their silent and symptomatic episodes were similar to the 94 (49%) patients without infarction, except for a longer duration of the silent episodes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrocardiographically and symptomatically silent myocardial ischemia during exercise testing

Certain patients with coronary artery disease (CAD) may have neither ST depression nor chest pain during exercise despite the presence of myocardial ischemia. The frequency and characteristics of such electrocardiographically and symptomatically silent ischemia were studied in 171 patients with both angiographically documented CAD and scintigraphically documented ischemia. Fifty-six (33%) of 171 patients had neither ST depression nor chest pain (Group N), and 115 (67%) had ST depression and/or chest pain (Group P). The two groups were similar with respect to age, gender, the prevalence of prior infarction, and peak systolic blood pressure. Group N patients, however, had a higher mean peak heart rate and rate-pressure product, less severe scintigraphic ischemia, a lower lung thallium-201 uptake, and a smaller number of diseased vessels. Stepwise discriminant analysis showed a history of effort angina, lung thallium-201 uptake, and scintigraphic severity of ischemia to be significant discriminators between Groups N and P. In conclusion, electrocardiographically and symptomatically silent ischemia may be common during exercise in patients with CAD, and less severe ischemia may be one of important determinants.     

Effects of daily high-intensity exercise on myocardial perfusion in angina pectoris

Forty male patients with chronic stable angina pectoris and no prior myocardial infarction were studied by planar thallium scintigraphy with use of circumferential profile analysis. Ischemic defects were assessed by measuring degrees of circumference involved and area of defect. Data were collected for 3 vascular regions in each of 3 views (anterior, 45 ° and 65 ° left anterior oblique projection). Patients were then randomized to exercise and control groups, the former training for a period of 1 year using the Canadian Airforce plan for physical fitness. After 1 year, both groups were restudied. Exercise training produced a 34% reduction in degrees of ischemia overall (p < 0.02), the most significant change being seen on the anterior view (72 ° ± 59 ° before vs 30 ° ± 35 ° after training). Regional analysis showed markedly improved perfusion anterolaterally and apically on the anterior view and anteroseptally on the 65 ° left anterior oblique view. These improvements support the hypothesis that exercise training improves myocardial perfusion by enhanced collateral function.     

Active transient myocardial ischemia during daily life in asymptomatic patients with positive exercise tests and coronary artery disease

The management of asymptomatic patients with coronary artery disease (CAD) is controversial, and the level of "activity" of their CAD during normal daily life remains largely unknown. To examine this question, ambulatory Holter monitoring of ST segments was performed out of the hospital in 7 asymptomatic subjects with CAD during normal daily activities. Their condition was detected because they all had a silent positive exercise test and angiographically proved CAD. During a total of 384 hours of monitoring, 37 asymptomatic episodes of ST depression (1 mm or greater and lasting at least 30 seconds) were recorded in 5 of the patients. Most episodes (68%) were 10 minutes or less in duration but ranged from 1 to 253 minutes, and most (70%) had a maximal ST depression of 1 to 2 mm. A small increase in heart rate, ranging from 1 to 34 beats/min, preceded 65% of the episodes, but 35% were associated with no change or even a decline before the onset of ischemia. Fifty-four percent of the episodes occurred during rest or usual light physical activity, 8% during sleep and only 38% during exercise, including 1 prolonged bout while jogging. During 78% of the episodes, the subjects rated their mental activity as usual and only 14% occurred during mental stress. In addition, a distinct diurnal variation was noted with 57% of the ischemia occurring between 0600 and 1200 hours (p = 0.008). Therefore, most asymptomatic subjects had active transient ischemia during daily life, with many of the characteristics already described in symptomatic subjects with CAD.     

缺血期急性高血糖对大鼠心肌缺血/再灌注损伤的影响

目的 探讨缺血期急性高血糖对大鼠心肌缺血/再灌注(MI/R)后心肌损伤的影响,并分析血糖水平与心肌损伤之间的关系.方法 在制备急性大鼠MI/R(缺血30min,再灌注6h)模型的基础上,静脉输注高浓度的葡萄糖溶液,造成2个不同浓度的缺血期急性高血糖动物模型.将32只SD大鼠随机平均分配为4组:(1)假手术组(SHAM),(2)生理盐水对照组(CON),(3)高糖1组(HG1)和(4)高糖2组(HG2).术中监测血糖水平,再灌注结束后检测心肌酶谱水平和心肌梗死面积(IS).结果 (1)与CON组相比较,HG1组和HG2组缺血期血糖水平均显著升高,分别为(10.5±1.0)、(18.0±1.2)mmol/L vs(4.7±0.7)mmol/L(P<0.05).(2)HG1组和HG2组的血肌酸激酶和乳酸脱氢酶水平明显升高,且心肌酶谱与血糖水平存在正相关(r分别为0.80和0.73,P<0.01).(3)HG1组的IS较CON组有扩大趋势,但差异无统计学意义[(40.8±5.2)%vs(37.6±5.8)%,P>0.05),HG2组的IS明显扩大[(45.6±8.5)%v8(37.6±5.8)%,P<0.05],且IS与血糖水平存在正相关(r=0.57,P<0.01).结论 缺血期急性高血糖加重大鼠MI/R损伤,且血糖水平与心肌酶谱和IS之间存在正相关.     

Effects of inosine on glycolysis and contracture during myocardial ischemia

The effects of inosine (INO) on substrate metabolism and rigor formation in ischemic myocardium were examined in isolated rabbit hearts. Metabolite content was assessed in tissue extracts by chemical analysis and in the whole heart by 13C and 31P nuclear magnetic resonance spectroscopy. In ischemic hearts metabolizing either [3-13C]pyruvate or [1-13C]glucose, 1 mM INO increased both total and 13C-labeled alanine content; lactate content was unaffected. At 3 minutes of ischemia, tissue alanine was 1.81 +/- 0.11 microM/g wet wt (mean +/- SEM) in hearts perfused with pyruvate+INO versus 1.23 +/- 0.15 microM/g wet wt in hearts perfused with pyruvate alone (p less than 0.05). INO reduced tissue glycogen during ischemia in pyruvate-perfused hearts. Tissue alanine content in ischemic hearts that were supplied glucose+INO (1.29 +/- 0.13 microM/g wet wt) was greater than in ischemic hearts supplied glucose alone (0.65 +/- 0.14 microM/g wet wt). Alanine was found to originate from pyruvate and was a glycolytic end product in glucose-perfused hearts. INO raised the [3-13C]alanine/[3-13C]lactate ratio in ischemic, intact hearts (glucose = 0.24 +/- 0.07 versus glucose+INO = 0.60 +/- 0.09; pyruvate = 0.49 +/- 0.08 versus pyruvate+INO = 0.89 +/- 0.08). At 7 minutes of ischemia, ATP content fell to 70 +/- 3% with glucose+INO versus 58 +/- 5% with glucose alone. Rigor (stone heart) was delayed from 14.7 +/- 1.3 to 23.2 +/- 1.6 minutes with INO. INO did not change ATP content in ischemic hearts that were supplied pyruvate but delayed rigor (pyruvate = 9.9 +/- 1.2 minutes; pyruvate+INO = 15.6 +/- 1.0 minutes), possibly at the expense of glycogen. Supplemental glucose improved the effectiveness of INO with pyruvate to preserve ATP (pyruvate+glucose = 42 +/- 6%; pyruvate+glucose+INO = 72 +/- 6%) and further delayed rigor (pyruvate+glucose = 13.3 +/- 1.5 minutes; pyruvate+glucose+INO = 20.3 +/- 1.8 minutes). Glucose metabolism supported improved energetic and contractile states in ischemic hearts treated with INO. Thus, cardioprotection of the ischemic heart by INO was associated with preservation of functional integrity and improved energy production due to increased glycolytic activity. Activation of glycolysis in the presence of INO was accommodated by augmented alanine production without the additional accumulation of lactate.     

Effects of ischemia, bypass surgery and past infarction on myocardial contraction, relaxation and compliance during exercise

Abnormalities of left ventricular function during ischemia have been described in animal models and in humans. Exercise, while a physiologic means of inducing ischemia, has a complex effect on left ventricular function by itself. In addition, patients with coronary artery disease have a diversity of chronic changes in myocardial structure and function. Therefore, with use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise was studied in 57 patients. Exercise-induced ischemia produced a decrease in ejection fraction, an increase in end-systolic volume, dramatic increases in diastolic pressures and an upward shift in the diastolic pressure-volume relation. Central to these changes was abnormal myocardial contraction and relaxation, with reduced regional shortening and impaired left ventricular pressure decay. However, nonischemic areas were capable of augmented shortening, and global pressure decay did accelerate slightly. These findings demonstrate that exercise-induced adjustments in contraction and relaxation are intertwined with ischemia-related abnormalities. Exercise studies in patients after bypass surgery and in patients with scars from distant myocardial infarction were useful in clarifying confounding factors. For example, asynchrony of contraction and relaxation, and chronic changes in passive chamber properties, also compromise systolic and diastolic function during exercise. In patients with coronary artery disease without ischemia during exercise, left ventricular end-diastolic pressure, but not early diastolic pressure, increased during exercise. The increase in pressure was appropriate for a slight increase in end-diastolic volume in a ventricle with a steep pressure-volume relation. Furthermore, end-systolic volume, while maintained during exercise, was not reduced, as occurs normally.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the prognostic values of ischemia during daily life and ischemia induced by treadmill exercise testing

Although silent ischemia is common in patients with stable coronary artery disease (CAD), controversy surrounds the issue regarding the most appropriate method for detection. Routinely performed exercise tolerance testing provides important prognostic information. However, ambulatory etectrocardiographic monitoring (AEM) has the distinct advantage of enabling evaluation of silent ischemia during daily life. Although numerous AEM studies have found a greater occurrence of silent ischemia than symptomatic ischemia in patients with stable angina pectoris, the independent prognostic value of AEM findings has not been definitively established. Several recent studies have addressed the question of whether AEM supplies additional information beyond that obtained from exercise testing. The results of these studies revealed that myocardial ischemia during daily life that is detected by AEM provides additional and independent prognostic information in patients with stable CAD who have evidence of ischemia during exercise testing.     

Transient myocardial ischemia during daily life in patients with syndrome X

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 ± 18 vs 117 ± 18 beats/min, p < 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, (1) myocardial ischemia frequently develops during daily life; (2) silent ischemia is an important component of this syndrome; and (3) increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.     

Effect of nisoldipine on exercise performance in heart failure following myocardial infarction.

The effects of the second generation calcium channel blocking drug nisoldipine on subjective and objective measurements of exercise performance were studied in 19 patients with moderate to severe heart failure (9 New York Heart Association functional class 2, 9 class 3 and 1 class 4) due to fixed ventricular dysfunction following myocardial infarction. Nisoldipine (10 mg 3 times daily) or placebo were administered for 8 weeks in a double-blind parallel study, assessing exercise performance by symptom-limited treadmill exercise testing using a modified Naughton protocol. Nisoldipine was well-tolerated and produced a small increase in peak estimated workload performed (6.2 +/- 2.9 to 8.2 +/- 3.0 METs, p = 0.06). The rate of perceived exertion (Borg scale) increased from 17.5 +/- 2.2 to 18.8 +/- 1.2 (p less than 0.02). The higher workload was performed at a lower peak systolic blood pressure (p = 0.03), higher peak heart rate (p = 0.06) and identical double product (NS). There was no change in resting and peak heart rate and blood pressure or in exercise performance in patients receiving placebo. Resting left ventricular ejection fraction, measured by radionuclide ventriculography, was unchanged after 8 weeks both in the placebo (21 +/- 9 to 20 +/- 9%) and nisoldipine (34 +/- 17 to 36 +/- 19%) groups.     

Similarity between women and men in manifestation of myocardial ischemia during exercise

We assessed the effect of gender on the electrocardiographic changes and thallium-201 myocardial perfusion during exercise in patients with coronary artery disease. Eighty-nine patients with coronary artery disease (50% or greater diameter narrowing of one or more major coronary arteries) who had undergone exercise thallium scintigraphy were retrospectively studied. There were 29 women and 60 men. Fifty-six patients had one-vessel disease, 11 patients had two-vessel disease, and 22 patients had three-vessel disease or left main disease. The extent of coronary artery disease was assessed by the Gensini score. There was no difference between men and women in age, medications, number of diseased vessels and the coronary artery disease score. Exercise tolerance was lower, although insignificantly in women compared to men. However, exercise heart rate, double product, and the electrocardiographic response were similar in men and women. Also, both the presence and size of exercise-induced perfusion defects were similar in men and women. Thus, the electrocardiographic response to exercise is not influenced by gender in patients with similar extent of coronary artery disease and comparable manifestations of myocardial ischemia.     

Transient ST-segment depression as a marker of myocardial ischemia during daily life

Patients with angina and coronary artery disease (CAD) have many episodes of transient ST-segment depression during ordinary daily life, and these are often asymptomatic. To investigate this signal as a marker of myocardial ischemia, 30 patients with chronic stable angina and CAD underwent positron tomography, recording the regional myocardial uptake of rubidium-82, pain and ST-segment changes before, during and after 59 technically satisfactory exercise tests, 35 cold pressor tests and 22 episodes of unprovoked ST depression. Exercise resulted in 53 episodes of ST depression with angina and in 5 episodes without pain. After cold pressor tests, there were 3 episodes of ST depression and pain and 12 of painless ST depression. Only 9 episodes of unprovoked ST depression were accompanied by pain. Tomography showed independent evidence of ischemia in 63 (97%) of the total 65 episodes of ST depression with angina and in all 30 episodes of painless ST depression. In each patient perfusion defects occurred in the same myocardial segment during painful and painless ST depression and responses were significantly different from those in 16 normal subjects studied in the same way. These findings support the use of transient ST depression in continuous monitoring to assess the activity of CAD, but only in patients with typical angina pectoris, ST depression during exercise and proved CAD. They strengthen the evidence derived from ambulatory monitoring for a wider picture of the disease than is generally appreciated, with more frequent episodes of silent myocardial ischemia than of angina pectoris.     

Symptomatic and silent myocardial ischemia during exercise testing in coronary artery disease

During exercise by patients with coronary artery disease (CAD), electrocardiographic evidence of myocardial ischemia may precede the onset of angina or may be unassociated with angina, even at peak levels of stress. However, neither the precise incidence of silent versus symptomatic ischemic episodes nor their interrelation in this setting has been clearly defined. The prevalence of silent and symptomatic myocardial ischemia during treadmill exercise testing was determined in 92 patients with angiographically documented CAD. The study group comprised 77 men (84%) and 15 women (16%) of mean age 57 years (range 32 to 79). Exercise testing resulted in ischemic ST-segment depression (greater than or equal to 1 mm for greater than or equal to 80 ms) only or in association with delayed (greater than or equal to 1 minute) angina in 39 patients (42%); angina only or in association with delayed ST-segment depression occurred in 42 patients (46%); and simultaneous occurrence of angina and ST-segment depression was noted in 11 patients (12%). Analysis of clinical, exercise and angiographic factors (age, sex, history of myocardial infarction, heart rate, maximal ST-segment depression, extent of CAD and left ventricular ejection fraction) revealed no significant correlation with the frequency of symptomatic and silent myocardial ischemia during exercise. Asymptomatic myocardial ischemia occurred commonly during exercise in patients with CAD, but there were no differences in the characteristics of patients with symptomatic and asymptomatic episodes.     

Effect of the calcium antagonist nisoldipine on coronary circulation and myocardial ischemia in temporary coronary occlusion

Sixteen patients undergoing PTCA of a significant lesion of the left anterior descending coronary artery received either 0.3 mg nisoldipine or placebo intravenously. Immediately before and during balloon inflation the following parameters were measured: aortic pressure, post-stenotic pressure, coronary occlusion pressure, diastolic pulmonary artery pressure, coronary sinus flow (thermodilution), and intracoronary ECG. After placebo there were no statistically significant changes. Nisoldipine led to a decrease in aortic pressure from 109 +/- 12 to 93 +/- 11 mm Hg (p less than 0.05) before, and from 103 +/- 14 to 92 +/- 8 mm Hg (NS) during balloon inflation. In contrast, coronary occlusion pressure remained unchanged. Heart rate increased from 80 +/- 13 to 96 +/- 16/min before (p less than 0.05), and from 87 +/- 18 to 97 +/- 17/min during balloon inflation (NS). Coronary sinus flow was increased from 95 +/- 16 to 116 +/- 13 ml/min before balloon inflation (p less than 0.01), and from 70 +/- 25 to 86 +/- 26 ml/min during balloon inflation (NS). ST-segment depression or elevation, severity of angina pectoris, and the diastolic pulmonary artery pressure remained unchanged. Thus, 0.3 mg nisoldipine led to a peripheral vasodilatation. While the aortic pressure decreased, coronary occlusion pressure remained unaffected. This could be explained by a marked dilatation of collateral vessels due to nisoldipine. However, myocardial ischemia remained unaffected as a result of the constant coronary occlusion pressure.     

Myocardial ischemia during daily activities: the importance of increased myocardial oxygen demand

The role of increased myocardial oxygen demand in the pathophysiology of myocardial ischemia occurring during daily activities was evaluated in 50 patients with coronary artery disease and exercise-induced ST segment depression. Each patient underwent ambulatory electrocardiographic (ECG) monitoring for ST segment shifts during normal daily activities and symptom-limited bicycle exercise testing with continuous ECG monitoring. All 50 patients had ST depression greater than or equal to 0.1 mV during exercise. A total of 241 episodes of ST depression were noted in the ambulatory setting in 31 patients; only 6% of these were accompanied by angina pectoris. Significant (0.1 mV) ST depression during ambulatory monitoring was preceded by a mean increase in heart rate of 27 +/- 12 beats/min. Patients with ischemia during daily activities developed ST depression earlier during exercise (7.9 +/- 4.4 vs. 14.2 +/- 6.4 min, p less than 0.001) and tended to have significant ECG changes at a lower exercise heart rate and rate-pressure product than did those without ST depression during ambulatory monitoring. In the 31 patients with ischemia during daily activities, the mean heart rate associated with ST depression in the ambulatory setting was closely correlated with the heart rate precipitating ECG changes during exercise testing (r = 0.74, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)