Onset Of ST-segment Depression Research Articles

Cardiovascular magnetic resonance signs of ischemia in hypertrophic cardiomyopathy

Background Recurrent myocardial ischemia has been recognized as playing an important role in the pathophysiology of hypertrophic cardiomyopathy (HCM) and cardiovascular magnetic resonance (CMR), with or without gadolinium, is a promising method of evaluating fibrosis, edema and hypoperfusion. The aim of this study is to evaluate the interrelationship between late enhancement (LE) and other signs of ischemia, such as edema and perfusion defects, and to relate them to clinical data in order to describe the stage of the disease. Methods Forty-four patients were evaluated by CMR cine images, T2-weighted sequences for edema and LE sequences. First-pass perfusion study was obtained in 37 patients. Acute-subacute ischemic events were clinically defined as the presence of chest pain or new onset of ST-segment depression, end-stage phase by left ventricular ejection fraction < 50% and maximal left ventricular wall thickness < 25 mm. Results Intramural patchy LE was found in 35/44 (80%) patients; extensive LE in 4/44 (9%). Edema was present in 24/44 (54%) patients and perfusion defects in 17/37 (46%). Simultaneous presence of patchy LE, edema and hypoperfusion in corresponding segments, was significantly associated to acute–subacute ischemic-phase parameters ( p = 0.02; RR 1.99, 95% C.I. 0.77–5.02). Extensive LE and perfusion defects in the absence of edema were significantly related to end-stage HCM ( p < 0.001; RR 13.7, 95% C.I. 1.83–102.05). Conclusions Using CMR in patients with HCM, we found focal tissue abnormalities consistent with regional ischemia at various stages. CMR provides important, clinically relevant information on the acuity, extent and functional relevance of ischemic injuries in HCM.

Prevalence and prognostic significance of silent myocardial ischemia in patients after myocardial infarction

Silent myocardial ischemia (MI) can be detected in subjects with any symptoms, in patients after myocardial infarction and in coronary patients who have episodes of symptomatic, as well as of silent MI. This study was carried out to evaluate the frequency, characteristics and prognostic significance of silent MI detected in stress echocardiography test in patients after myocardial infarction. In 210 patients within three months after myocardial infarction exercise test was performed. In those patients with ischemic ST depression on exercise electrocardiogram, in order to confirm MI stress echocardiography was additionally performed. To assess the incidence of major cariovascular events, all the patients were followed at least five years after the first myocardial infraction. Out of 210 patients 88 (42%) had ischemic response during stress echocardiography test. Out of 88 patients with MI 54 (61%) had anginal pain (patients with symptomatic MI), while 34 (39%) were free of symptoms (patients with silent MI). Level of exercise test, heart rate, time to the onset of ST segment depression, and the magnitude of ST segment depression were similar in both subgroups of the patients with MI. Duration of exercise test was longer in patients with silent MI (p < 0.05). Wall motion score index during stress echocardiography was higher in patients with symptomatic MI (p < 0.05). Coronary angiography findings were similar in patients with silent and those with symptomatic MI. During a five-yearsfollow-up period the occurrence of major cardic events (cardiac mortality and recurrent myocardial infarction) was similar in both subgroups of the patients with MI. In more than one third of patients after myocardial infarction silent MI during stress echocardiography was detected. The patients with silent ischemia had longer duration of exercise test and smaller wall motion score index on stress echocardiography. There was no difference in coronary angiography finding between patients with silent and those with symptomatic MI. The incidence of major cardiac events during a five- years- follow-up was similar in the patients with silent and those with symptomatic MI.

A Randomized, Double-Blind Comparison of Lercanidipine 10 and 20 mg in Patients with Stable Effort Angina

We evaluated the antiischemic action and the effects on left ventricular response to exercise of lercanidipine, a long-acting dihydropyridine calcium antagonist, in 23 patients with stable effort angina in a randomized, double-blind, parallel trial. Left ventricular function was assessed during upright bicycle exercise using an ambulatory radionuclide detector for continuous noninvasive monitoring of cardiac function. Exercise was performed under control conditions before (run-in placebo period) and after 2-week treatment with lercanidipine 10 or 20 mg once daily. During the placebo run-in period and at the study end, patients underwent clinical examination, ECG, exercise tests, ambulatory ventricular scintigraphic monitoring (VEST). Results showed that both drug doses increased time to onset of ST segment depression >/=1 mm and peak ST segment depression, with improvement of total exercise duration. Heart rate, blood pressure, and the rate-pressure product did not significantly change with respect to pretreatment value. The left ventricular ejection fraction, indicating contractility state of myocardium, was unchanged at rest and during exercise after both lercanidipine doses. In conclusion, lercanidipine is safe and effective in reducing ischemia in patients with stable effort angina without any deterioration of cardiac function.

Effect of intravenous testosterone on myocardial ischemia in men with coronary artery disease

Background Studies on the effect of estrogen on atherosclerotic coronary artery disease (CAD) risk in women have produced conflicting results. Similar confusion, but fewer data, exists on the effect of testosterone on CAD risk in men. Methods We used 99mTc sestamibi single-photon emission computed tomography (SPECT) myocardial perfusion imaging to examine the acute effect of intravenous testosterone in 32 men (mean age, 69.1 ± 6.4 years) with provocable myocardial ischemia on standard medical therapy. Patients performed 3 exercise (n = 18) or adenosine (n = 16) stress tests during the infusion of placebo or 2 doses of testosterone designed to increase testosterone 2 or 6 times baseline. Results Serum testosterone increased 137 ± 58% and 488 ± 113%, and estradiol levels increased 27 ± 46% and 76 ± 57%, (P <.001 for all) during the 2 testosterone infusions. There were no differences among the placebo or testosterone groups in peak heart rate, systolic blood pressure, maximal rate pressure product, perfusion imaging scores, or the onset of ST-segment depression. Conclusions Acute testosterone infusion has neither a beneficial nor a deleterious effect on the onset and magnitude of stress-induced myocardial ischemia in men with stable CAD. (Am Heart J 2002;143:249-56.)

Placebo effect in clinical trials

It is well known that placebos evoke a variety of effects in the human body. It is less known that placebo medication can produce adverse drug reactions (ADRs). The efficacy and, as the main topic, the tolerability were investigated from an international clinical data pool on placebo-controlled randomized multicenter studies of 5 different groups of indications. The therapeutic areas analyzed were neuropsychiatry (nimodipine, ipsapirone), cardiology (nisoldipine), metabolism (acarbose) and gastroenterology (hydrotalcit). The placebo efficacy was evident and varied not only in comparison to 5 indication groups analyzed, but also within them. Placebo showed for example hardly an effect on the symptomatology of stroke patients with a severe neurological deficit in comparison to verum while there was a 50% improvement in symptoms following placebo application in patients with a mild stroke. In angina patients exercise tolerance increased under placebo by 10% (time to onset of ST segment depression and symptoms of angina) while verum showed a 22% improvement. In diabetes placebo had no effect as compared to baseline and to a verum on blood glucose and HbA1C. ADRs could be observed under placebo treatment. The frequency and kind of placebo-induced ADRs varied also between the indication groups, i.e. typical CV side-effects were observed in CV controls. The placebo ADR profile was similar to the reference drug also. Some ADRs were reported even more frequently under placebo than under verum, like "dry mouth" in patients with general anxiety status. Placebo therapy is frequently effective and is not a "non-therapy". Placebo effects can be shown only by direct comparison with a "non-therapy". A placebo therapy is frequently accompanied by adverse drug reactions (ADRs) just as a verum therapy. Placebo ADRs are frequently illness- and verum-specific. Effects and ADRs of placebo therapy must be known, to judge the effect of verum medication in controlled clinical trials. The mechanisms of placebo effects are manifold (e.g. endorphine release, conditioned learning). Since placebo therapy outside of evidence-based medicine (use of drugs without proven efficacy = pseudoplacebos) may potentially also cause serious side effects, the use may not only be useless but also harmful.

Blood Pressure Changes During Transient Myocardial Ischemia: Insights Into Mechanisms

Objectives. We investigated the contribution of changes in systemic blood pressure to the genesis of spontaneous myocardial ischemia.Background. Although increases in heart rate often precede the development of spontaneous myocardial ischemia, it remains a subject of controversy whether these are accompanied by simultaneous changes in blood pressure.Methods. Using an ambulatory monitoring device that triggered blood pressure recordings from the level of the ST segment, we documented systolic and diastolic blood pressure and heart rate changes related to episodes of ST segment depression in 17 patients with stable coronary artery disease.Results. Systolic blood pressure and heart rate, but not diastolic pressure, increased significantly before the onset of ST segment depression and persisted throughout the ischemic episode. There was a significant correlation between the changes in heart rate and systolic blood pressure during episodes of myocardial ischemia (r = 0.5, p = 0.0005) and between heart rate and systolic blood pressure changes at 1-mm ST segment depression during treadmill exercise testing and ambulatory monitoring (r = 0.73, p = 0.0005 for heart rate; r = 0.77, p = 0.0008 for systolic blood pressure), indicating that patients with a low heart rate threshold during ischemic episodes also had a lower systolic blood pressure threshold before ischemia during both tests. Circadian changes in systolic blood pressure paralleled the variations in heart rate and ischemic episodes, with the lowest values at night.Conclusions. Significant increases in myocardial oxygen demand, including systolic blood pressure, occur during episodes of spontaneous myocardial ischemia. Patients with a lower heart rate threshold during ischemic episodes had a lower systolic blood pressure threshold during both ambulatory monitoring and treadmill exercise. The effects of antianginal therapy on blood pressure changes during ischemia need to be explored further.

A Reappraisal of Exercise Electrocardiographic Indexes of the Severity of Ischemic Heart Disease: Angiographic and Scintigraphic Correlates

Objectives. We explored how the exercise electrocardiographic (ECG) indexes generally presumed to signify severe ischemic heart disease (IHD) correlate with coronary angiographic and scintigraphic myocardial perfusion findings.Background. In exercise testing, it is generally assumed that the early onset of ST segment depression and its occurrence at a low rate–pressure product (ischemic threshold); the amount of maximal ST segment depression; and a horizontal or downsloping ST segment and its prolonged recovery after exercise signify more severe IHD. However, the relation of these indexes to coronary angiographic and exercise myocardial perfusion findings in patients with IHD is unclear.Methods. We prospectively carried out a symptom-limited 12-lead Bruce protocol thallium-201 single-photon emission computed tomographic (SPECT) exercise test in 66 consecutive subjects with stable angina, ≥70% stenosis of at least one coronary artery, normal rest ECG and left ventricular wall motion and a prior positive exercise ECG. The above ECG indexes, vessel disease (VD), a VD score and the quantitative thallium-SPECT measures of the extent, maximal deficit and redistribution gradient of the perfusion abnormality were characterized.Results. Maximal ST segment depression could not differentiate the number of diseased vessels; was not related to VD score, maximal thallium deficit or redistribution gradient; but was related to the extent of perfusion abnormality (r = 0.29, 95% confidence interval [CI] 0.08 to 0.52, p = 0.02). Time of onset of ST segment depression correlated inversely only with VD (r = −0.22, 95% CI −0.44 to −0.05, p < 0.05), whereas the ischemic threshold had low inverse correlation only with VD score (r = −0.25, 95% CI −0.47 to −0.01, p < 0.05) and the redistribution gradient (r = −0.33, 95% CI −0.53 to −0.10, p < 0.01). A horizontal or downsloping compared with an upsloping ST segment did not demonstrate more severe angiographic and scintigraphic disease. Recovery time did not correlate with angiographic and scintigraphic findings, and correlations between angiographic and scintigraphic findings were also low or absent.Conclusions. In this homogeneous study group, the exercise ECG indexes did not necessarily signify more severe IHD by angiographic and scintigraphic criteria. Lack of concordance between the exercise ECG, angiography and myocardial scintigraphy suggests that these diagnostic modalities examine different facets of myocardial ischemia, underscoring the need for caution in the interpretation of their results.(J Am Coll Cardiol 1997;29:1497–504)

William Heberden Revisited: Postprandial Angina—Interval Between Food and Exercise and Meal Composition Are Important Determinants of Time to Onset of Ischemia and Maximal Exercise Tolerance

Objectives. This study aimed to explore the hemodynamic responses to ingestion of meals of different composition in patients with chronic stable angina and to assess the effect of these meals on time to onset of >1-mm ST segment depression and limiting angina pectoris during exercise.Background. To our knowledge, no study has assessed the effect of meal composition and timing of exercise in patients with coronary artery disease.Methods. Fifteen patients with chronic stable angina visited our laboratory in the fasted state on three occasions. Measurements of cardiac output, heart rate and blood pressure were taken while patients were standing. A modified Bruce exercise test was then carried out, during which time to onset of >1-mm ST segment depression and limiting chest pain were recorded. Patients then ate a 2.5-MJ high fat or high carbohydrate meal; on the third occasion, no meal was taken. At 30 min and 1 h after eating the meals, rest hemodynamic measurements and exercise tests were repeated.Results. The high fat meal did not affect exercise variables, whereas the high carbohydrate meal resulted in a reduction in time to onset of ST segment depression of 74.4 ± 22.2 s (mean ± SEM) during exercise at 30 min (p < 0.01), and at both 30 and 60 min after the high carbohydrate meal, limiting chest pain occurred 50 to 90 s earlier than when patients fasted (p < 0.01).Conclusions. One hour after a high carbohydrate meal, the onset of angina during exercise occurs earlier than in the fasted state. Despite similar hemodynamic adjustments, a high fat meal does not affect exercise time.(J Am Coll Cardiol 1997;29:302–7)

Usefulness of the transcendental meditation program in the treatment of patients with coronary artery disease

Twenty-one patients with documented coronary artery disease were tested at baseline by exercise tolerance testing, and assigned to either stress reduction using the Transcendental Meditation (TM) program or to a wait-list control, After 8 months, the TM group had a 14.7% increase in exercise tolerance, an 11.7% increase in maximal workload, an 18% delay in onset of ST-segment depression, and significant reductions in rate-pressure product at 3 and 6 minutes, and at maximal exercise compared with the control group.

Left ventricular functional reverse in patients with syndrome X: Evaluation by continuous ventricular function monitoring

Objectives. The objective of this study was to evaluate cardiac functional reserve in patients with syndrome X.Background. Syndrome X is characterized by stress-induced anginal pain and ST segment depression, normal findings on coronary angiography and normal left ventricular function at rest. Reduced coronary vasodilative reserve and abnormal myocardial lactate metabolism have been described in such patients.Methods. To assess left ventricular functional reserve in patients with syndrome X, continuons radionuclide monitoring of left ventricular end-diastolic volume, end-systolic volume and ejection fraction was performed in 12 patients and 13 normal control subjects during supine bicycle ergometer exercise.Results. In control subjects, end-diastolic volume increased at peak exercise from 100% to 106.5% (p < 0.01), end-systolic volume decreased from 39.1% to 22.6% (p < 0.01) and ejection fraction increased from 60.9% to 78.6% (p < 0.01). In patients with syndrome X, end-diastolic volume increased at peak exercise from 100% to 106% (p < 0.01), and end-systolic volume decreased at ST segment depression ≤0.5 mm (the ST point) from 37% to 28.8% (p < 0.01) but increased at peak exercise to 44.7% (p < 0.01 vs. the ST point). Thus, ejection increased at the ST point from 63% to 72.7% (p < 0.01) but decreased at peak exercise to 57.7% (p < 0.01 vs. the ST pint and control subjects) in proportion to the degree of ST segment depression. In nine patients (75%), ejection fraction at peak exercise was lower than baseline values. All patients and control subjects showed a rapid ejection fraction increase just after exercise during the recovery period. The degree of ejection fraction “overshoot” in patients was similar to that in control subjects, but the interval from the end of exercise to the overshoot in patients was significantly longer than that in control subjects (118 vs. 65 s, p < 0.01).Conclusions. In patients with syndrome X subjected to exercise stress, left ventricular function remained normal before the onset of ST segment depression. Once ST segment depression appeared, left ventricular function deteriorated in proportion to the degree of depression, and reduced left ventricular function persisted into the recovery period. Continuous ventricular function monitoring is thus a useful predictor of reduced left ventricular functional reserve in patients with syndrome X.

Role of increases in heart rate in determining the occurrence and frequency of myocardial ischemia during daily life in patients with stable coronary artery disease

Objectives. The goal of this study was to investigate the role of increases in heart rate in the development of ischemic episodes recorded during ambulatory electrocardiographic (ECG) monitoring in patients with stable coronary artery disease and to establish the importance or such increases in determining the frequency of ambulatory myocardial ischemia.Background. The factors that determine the occurrence and frequency of episodes of myocardial ischemia that patients with stable coronary artery disease experience during daily life have not been clearly defined. In particular, the role of increases in heart rate in the development of myocardial ischemia is controversial.Methods. To address these issues, 54 patients (42 men and 12 women, mean age 60.5 ± 8 years) with proved coronary artery disease who had ≥1 mm ST segment depression during exercise testing underwent an exercise treadmill test with use of the National Institutes of Health combined protocol and a 48-h period of ambulatory ECG monitoring. The exercise ischemic threshold was determined as the heart rate at the onset of ST segment depression during exercise testing.Results. During monitoring, 48 (89%) of the 54 patients had at least one episode of ST segment depression (mean ± SD 6.6 ± 5 episodes, range 0 to 22). The majority (320 of 359 or 89%) of ischemic episodes were preceded by an increase in heart rate ≥10 beats/min; the most significant increase (22.3 ± 10 beats/min) occurred during the 5-min period before the onset of the episode. An ischemic episode occurred 80% of the times the heart rate reached the exercise ischemic threshold. A strong correlation was observed between the number of times the exercise Ischemic threshold was reached during monitoring and both the number and the duration of ischemic episodes (r = 0.90 and 0.71, respectively, p < 0.0001).Conclusions. Increases in heart rate that exceed the exercise ischemic threshold are commonly observed before the onset of episodes of ambulatory myocardial ischemia in patients with stable coronary artery disease. Moreover, such increases constitute an important determinant of the frequency of myocardial ischemia during daily life. These findings may explain the variability observed in the number of ischemic episodes and may have important implications for the mechanisms that contribute to myocardial ischemia in daily life and for the clinical evaluation of patients with coronary artery disease.

Transient ST segment depression during holter monitoring: How to avoid false positive findings

To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a detailed shape analysis of real-time printouts to the usual criteria of significant ST segment depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of pathologic findings in preliminary examinations. The remaining 85 (49 women and 36 men; mean age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST segment depresion with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes). Supplementary criteria—e.g., sudden onset of ST segment depression, identical orientation of PQ and ST segments, or simultaneous increase in R and P wave amplitude—made it possible to identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true silent ischemia not be differentiated from false positive results. Thus consideration of only the extent, frequency, and duration of episodes does not permit a differentiation between true silent ischemia and false positive results. A supplementary shape analysis increases the specificity of ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.

Exercise-Induced Symptomatic and Asymptomatic Myocardial Ischemia in Patients with Severe Coronary Artery Disease: Focus on the Efficacy and Safety of Gallopamil

Symptomatic and asymptomatic episodes of transient myocardial ischemia are well-known risk factors in patients with coronary artery disease. In a single-blind, randomized, and placebo-controlled study, the efficacy and safety of gallopamil was studied during a 1-week treatment period in 25 patients with high-grade coronary artery stenosis and frequent, exercise-induced episodes of myocardial ischemia. Eighteen patients were men, and seven patients were women; the mean age +/- SD was 59 +/- 7 years. After a 1-week run-in period (days 1-7), all patients were treated with gallopamil 50 mg t.i.d. (days 8-14) and placebo t.i.d. (days 15-21) or vice versa. Twenty-four-hour Holter monitoring, exercise testing, and adverse effects were controlled at days 7, 14, and 21. During the run-in period, all patients suffered a mean of 5.9 +/- 2.9 episodes of transient myocardial ischemia, mean ischemic duration was 38 +/- 29 min/day. Gallopamil increased exercise tolerance from 7.9 to 9.8 min (+24%, p < 0.05) and resulted in reduction of the weekly usage of short-acting nitrates by 45% compared to placebo. During 24-h Holter monitoring, mean heart rate at the onset of ST-segment depression increased from 106 to 118 beats/min (p < 0.05). The frequency of daily ischemic episodes was reduced after gallopamil administration from 6.1 to 3.9 episodes/day (-37%, p < 0.05), the total ischemic burden decreased for symptomatic episodes by -54% (p < 0.05) and for asymptomatic episodes by 29% (p < 0.05). Gallopamil modified the circadian distribution of ischemic episodes by modifying the morning peak of transient myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Prediction of the frequency and duration of ambulatory myocardial ischemia in patients with stable coronary artery disease by determination of the ischemic threshold from exercise testing: Importance of the exercise protocol

The relation between ambulatory myocardial ischemia and the results of exercise testing in patients with ischemic heart disease remains undefined, because of the dissimilar results of previous reports. To further investigate this issue and, in particular, to ascertain the importance of the exercise protocol in determining that relation, 70 patients with stable coronary artery disease underwent 48 h ambulatory electrocardiographic (ECG) monitoring and treadmill exercise tests after withdrawal of medications. Patients exercised using two different protocols with slow (National Institutes of Health [NIH] combined protocol) and brisk (Bruce protocol) work load increments. Exercise duration was longer with the NIH combined protocol (14.1 +/- 5 versus 6.8 +/- 2 min; p less than 0.0001), but the maximal work load and peak heart rate achieved were greater with the Bruce protocol (9.8 +/- 2 versus 6.5 +/- 2 METs, and 142 +/- 19 versus 133 +/- 22 beats/min, respectively; p less than 0.0001). A close inverse correlation between exercise testing and the results of ambulatory ECG monitoring was observed using the NIH combined protocol; the strongest correlation was observed between time of exercise at 1 mm of ST segment depression and number of ischemic episodes (r = -0.86; p less than 0.0001). With the Bruce protocol a significantly weaker inverse correlation was found (r = -0.35). The mean heart rate at the onset of ST segment depression was similar during monitoring and during exercise testing with the NIH combined protocol (97.2 +/- 13 versus 101.0 +/- 17 beats/min, respectively) but it was significantly higher (110.4 +/- 13) when using the Bruce protocol (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Ability of calcium-entry blockade by felodipine to disclose different pathogenetic mechanisms behind hyperventilation-induced myocardial ischemia in men

To verify that myocardial ischemia occurring during ither the overbreathing or recovery phase of the hyperventilation test is based on different pathogenetic mechanisms, 2 consecutive series of patients, selected on the basis of their response to a run-in hyperventilation test, were studied. Group I comprised 15 patients who developed ST-segment depression early during overbreathing, whereas group II consisted of 12 patients showing ST-segment depression late during the recovery phase. A single oral dose of felodipine 10 mg or of placebo was administered on 2 consecutive days according to a randomized, double-blind, crossover design, and the hyperventilation test was repeated, on both days of the study, 3 to 5 hours after drug intake. In group I, ST-segment depression occurred after placebo in all patients during overbreathing, with an increase in rate pressure product (from 112 ± 31 at baseline to 168 ± 55 mm Hg × beats/min/100 at the onset of ST-segment depression; p < 0.01). After felodipine, 13 patients continued to show ST-segment depression during overbreathing, together with an increase in rate pressure product (from 107 ± 24 at baseline to 158 ± 46 mm Hg × beats/ min/100 at the onset of electrocardiographic changes; p < 0.01). In group II, all 12 patients showed ST-segment depression during recovery after placebo, with a rate pressure product comparable to baseline conditions (112 ± 35 at baseline vs 102 ± 27 mm Hg × beats/min/100 at the onset of ST-segment depression; difference not significant). After felodipine, no patient developed ST-segment depression or chest pain. These findings confirm that early hyperventilation-induced ST-segment depression is related to increased oxygen consumption, which cannot be prevented by felodipine. On the other hand, felodipine is highly effective in preventing delayed ischemia, which is due to a primary reduction in coronary blood flow.

Similar time course of ST depression during and after exercise in patients with coronary artery disease and syndrome X

To assess whether the time course of ST segment depression differs in patients with coronary artery disease and patients with angina and normal coronary arteries, the exercise tests of 54 patients with documented coronary artery disease and 25 patients with syndrome X (angina, positive exercise test, no evidence of coronary artery spasm, and normal coronary arteries) were compared. All tests were performed with therapy withheld, using the modified Bruce protocol. In each test, time, heart rate and blood pressure were measured at the onset and at 1 mm of ST segment depression, and at peak exercise. Recovery (return of the ST segment to baseline ±0.2 mm) time was also assessed. Peak ST segment depression was similar in coronary artery disease and syndrome X patients (1.5 ± 0.3 versus 1.6 ± 0.4 mm). In 42 coronary artery disease patients, ST segment depression developed early (≤6 minutes) during exercise; this was associated with a short recovery (≤3 minutes) in 17 (40%) and with a long recovery (>3 minutes) in 25 (60%) patients. In 17 patients with syndrome X, ST segment depression developed early; it was associated with a short recovery in six (35%) and with a long recovery in 11 (65%) patients. Late (>6 minutes) onset of ST segment depression was observed in 12 coronary artery disease patients; of these, eight (67%) had a short recovery and 4 (33%) had a long recovery. Late onset of ST segment depression occurred in eight patients with syndrome X; six (75%) had a short recovery and two (25%) had a long recovery. Average time, heart rate, and heart rate-blood pressure product were higher in syndrome X than in coronary artery disease patients, both at 1 mm of ST segment depression (618 ± 74 versus 468 ± 234 seconds, p < 0.01; 140 ± 19 versus 117 ± 22 beats/min, p < 0.001; and 239 ± 60 versus 193 ± 56 beats/min·mm Hg·10 −2, p < 0.05, respectively) and at peak exercise (708 ± 144 versus 546 ± 246 seconds, p < 0.01; 145 ± 18 versus 124 ± 23 beats/min, p < 0.001; and 256 ± 42 versus 213 ± 61 beats/min·mm Hg·10 −2, p < 0.05, respectively). One millimeter of ST segment depression developed at a heart rate ≤ 110 beats/min in 47% of coronary artery disease patients but in only 4% of syndrome X patients. Thus the time course of ST segment depression during exercise is similar in syndrome X and in coronary artery disease, but the heart rate at which diagnostic ST segment depression develops is significantly different in these two conditions.

Pathophysiology of silent myocardial ischemia during daily life. Hemodynamic evaluation by simultaneous electrocardiographic and blood pressure monitoring.

The role of myocardial oxygen demand in the genesis of silent myocardial ischemia was evaluated by measuring the heart rate and blood pressure changes preceding the silent ischemic events during daily life in 25 men with proven coronary artery disease. Simultaneous 24-48-hour ambulatory electrocardiographic and blood pressure monitoring were performed during unrestricted daily activities. Of the 92 transient ischemic events recorded during monitoring, 85 (92%) were silent. Sixty-one percent of the silent events were preceded by an increase in the heart rate of 5 beats/min or more. Seventy-three percent of the silent ischemic events showed an average increase of 10 mm Hg in systolic blood pressure within 6 minutes preceding the onset of ST segment depression. The silent ischemic events showed a circadian pattern with a high density (34% of total events) between 6:00 AM and noon. The increase in heart rate and blood pressure paralleled the increase in silent ischemic events during these hours. These results showing significant (p less than 0.001 for both) increases in heart rate and blood pressure preceding a majority of silent ischemic events suggest that increase in myocardial oxygen demand plays a significant role in the genesis of silent ischemia. This pathophysiological mechanism has important therapeutic implications.

Angina and ST-Segment Depression During Treadmill and Arm Ergometer Testing in Patients with Coronary Artery Disease

The clinical use of exercise rehabilitation programs has increased for patients with coronary artery disease. Exercise testing in these programs typically is conducted on a treadmill or cycle ergometer, although many patients' vocations require upper extremity activities and some patients cannot perform lower extremity exercises. To compare the hemodynamic responses and the incidence of angina and ST-segment depression during upper and lower extremity exercise in patients with coronary artery disease, we administered symptom-limited arm ergometer and submaximal or maximal symptom-limited treadmill tests to 95 cardiac rehabilitation patients who had completed an eight-week exercise training program. Treadmill testing resulted in significantly higher heart rates, systolic blood pressures, and double products than arm ergometer testing. The incidence of ST-segment depression was significantly greater with treadmill testing than with arm ergometer testing, but the incidence of angina was not different between tests. Ten patients had ST-segment depression during both arm ergometer and treadmill testing, and the double products at the onset of ST-segment depression were not different. Our data suggest that arm ergometer testing is less likely to result in ST-segment depression than treadmill testing in patients with coronary artery disease, possibly because of the lower hemodynamic responses during arm ergometer testing.

Effects of intracoronary isosorbide dinitrate during acute myocardial ischaemia: a study during angioplasty.

The effects of isosorbide dinitrate on acute myocardial ischaemia were studied in 19 patients during coronary angioplasty. The duration of balloon inflation to the onset of ST segment depression was increased by the administration of intracoronary isosorbide dinitrate from (mean +/- SEM) 13 +/- 2 to 20 +/- 2 s (48%) (P less than 0.01) and the duration to 1 mm ST segment depression increased form 23 +/- 2 to 29 +/- 3 s (28%) (P less than 0.01). Systolic blood pressure fell from 118 +/- 3 to 111 +/- 4 mmHg but there was no change in intracoronary distal occlusion pressure. Thus during coronary occlusion isosorbide dinitrate prolongs the time to the onset of myocardial ischaemia.

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.