ST-segment Depression In Patients Research Articles

ST-segment depression resolution predicts infarct size and reperfusion injury in ST-elevation myocardial infarction

ObjectiveST-elevation myocardial infarction (STEMI) is frequently associated with reciprocal ST-segment depression in contralateral ECG leads. However, the relationship of the resolution of ST-segment depression (STD-R) with myocardial damage is unknown...

Prevalence and Clinical Significance of Up-Sloping ST-Segment Depression in Patients With Non-ST-Segment Elevation Myocardial Infarction

BackgroundUp-sloping ST-segment depression has not been historically considered as representing ischemia as this electrocardiographic change can be seen in normal subjects during exercise stress testing or tachycardia. We aimed to clarify the prevalence and clinical significance of up-sloping ST-segment depression in patients with non-ST-segment elevation myocardial infarction (NSTEMI).MethodsWe performed a retrospective analysis of 330 consecutive patients with NSTEMI who underwent coronary angiography. ST-segment depression ≥ 0.05 mV in more than two contiguous leads was recorded and categorized as being up-sloping or non-up-sloping.ResultsOf 330 patients, 109 patients (33%) had ST-segment depression; six of these patients had up-sloping ST-segment depression. All six patients with up-sloping ST-segment depression had a culprit lesion and underwent in-hospital revascularization. Three of these six patients had a culprit lesion in the left anterior descending artery; the culprit lesion in two others was in the left circumflex artery, while one patient had severe three-vessel disease. No statistically significant difference was found in the rate of in-hospital revascularization between patients with up-sloping and non-up-sloping ST-segment depression (100% vs. 75%, P = 0.33).ConclusionsPatients with up-sloping ST-segment depression had a comparable rate of in-hospital revascularization compared to those with non-up-sloping ST-segment depression, suggesting that up-sloping ST-segment depression should be recognized as a manifestation of ischemia in NSTEMI.

The changes of inflammatory cytokines and their clinical significance in patients of inferior ST-segment elevation acute myocardial infarction with anterior ST-segment depression

To investigate the level of Hs-CRP, Fib,IL-6, TNF-α,MDA, SOD, and analyse the correlation between the level of plasma inflammatory cytokines and clinical significance in patients with anterior ST-segment depression. We choose 360 patients with inferior ST Segment elevation acute myocardial infarction from May 2007 to Sep 2012 in rescue Center of Anzhen Hospital, in Anzhen Hospital, and all the patients received percutaneous coronary intervention treatment and the vascular lesions besides culprit vessel were observed. All the patients were divided into two groups: control group (n = 180) and anterior ST-segment depression group (n = 180). 8ml venous blood was obtained from all the patients, and then plasma were separated. The level of plasma Hs-CRP, Fib, IL-6, TNF-α, MDA, SOD were investigated by Biochemistry and ELISA. And the relativity between the level of plasma inflammatory cytokines and anterior ST-segment depression in patients with inferior acute myocardial infarction was analysed. The proportion of double vessel coronary disease, three coronary artery lesion is higher in anterior ST-segment depression group compared with control group (P < 0.01) . Compared with control group, the level of Hs-CRP, Fib, IL-6, TNF-α,MDA, SOD of anterior ST-segment depression group are inclined significantly (P < 0.01). The level of plasma inflammatory cytokines and the degree of lipid peroxidation can reflect the severity of coronary artery disease and may have certain value in predicting the severity of disease.

Diagnostic Accuracy of Electrocardiographic ST-Segment Depression in Patients With Rapid Atrial Fibrillation for the Prediction of Coronary Artery Disease

BackgroundWe aimed to examine the diagnostic value of ST-segment depression in patients with rapid atrial fibrillation (AF) for the prediction of coronary artery disease (CAD). MethodsHemodynamically stable patients with AF, and a heart rate > 80% of their maximum predicted according to their age, were allocated to 2 groups according to their electrocardiographic findings on admission: group A included patients without any ST-segment abnormalities and group B, patients with downward or horizontal ST-segment depression ≥ 1 mm in 2 or more contiguous leads. Group A patients were subjected to a dobutamine stress echo or Tl-201 myocardial single-photon emission computed tomography, followed by coronary angiography in case of abnormal results and Group B patients to coronary angiography. CAD was defined angiographically as stenosis of ≥ 50% in any major epicardial coronary vessel. ResultsOut of 115 consecutive patients, with a mean age of 65.9 ± 10.2 years, 42.6% were male, 18.3% smokers, 68.7% hypertensive, 21.7% had diabetes, and 40% had hyperlipidemia. We enrolled 71 and 44 patients in group A and B, respectively. Prevalence of significant CAD among studied patients was 21.7%, 3/71 (4.2%) and 22/44 (50.0%) in group A and B, respectively. Overall ST-segment depression during rapid AF had 88.0% sensitivity (95% confidence interval [CI], 67.7%-96.8%) and 75.6% specificity (95% CI, 65.2%-83.7%) in predicting presence of CAD, and positive and negative predictive value was 50.0% (95% CI, 34.8%-65.2%) and 95.8% (95% CI, 87.3%-98.7%), respectively. ConclusionsIn consecutive patients with rapid AF, the absence of ST-segment depression might indicate absence of CAD.

Prognostic significance of reciprocal ST-segment depression in patients with acute STEMI undergoing immediate invasive intervention

PurposesReciprocal changes are frequent in patients with acute ST-segment elevation myocardial infarction (STEMI). However, their prognostic significance is not clear in patients undergoing immediate invasive intervention. Basic ProcedureWe retrospectively examined 165 consecutive patients with STEMI receiving immediate invasive intervention. The first electrocardiography taken in the emergency department was analyzed. Patients were assigned to 2 groups: with a reciprocal change (group I, n = 100) and without a reciprocal change (group II, n = 65). Main FindingsElectrocardiographs revealed that more anterolateral and inferior STEMI occurred in group I and more anterior STEMI occurred in group II. In the emergency department, group I had lower systolic and diastolic blood pressures, higher ventricular tachycardia and fibrillation rates, and higher cardiopulmonary resuscitation rates than did group II. Upon admission, peak troponin I levels were significantly higher in group I, and more group I patients required intra-aortic balloon pumping support. This unstable hemodynamic condition in group I patients was reflected by their higher in-hospital mortality rate. Multivariate analysis showed that age (odds ratio [OR], 1.103; 95% confidence interval [CI], 1.022-1.190; P = .012), Killip class (OR, 2.785; 95% CI, 1.049-7.400; P = .040), and reciprocal change (OR, 9.553; 95% CI, 1.146-79.608; P = .037) remained as independent predictors of in-hospital mortality. Actuarial freedom from all-cause mortality was worse in group I (P = .046). Principal ConclusionsThe data suggest that patients with STEMI with reciprocal electrocardiographic changes have unstable hemodynamic status and poorer outcomes. Further prospective studies using a larger patient population are needed.

Prognostic significance of electrocardiographic-determined left ventricular hypertrophy and associated ST-segment depression in patients with non–ST-elevation acute coronary syndromes

Left ventricular hypertrophy (LVH) is frequently associated with ST depression (STD) on the electrocardiogram (ECG), a so-called strain pattern. Although STD is a well-established adverse prognosticator in non-ST-elevation acute coronary syndrome (NSTE-ACS), the relative prognostic importance of LVH and associated STD has not been elucidated. A total of 7,761 patients with NSTE-ACS in the Global Registry of Acute Coronary Events (GRACE) and ACS-I registries had admission ECGs analyzed at a core laboratory. Left ventricular hypertrophy (determined by Sokolow-Lyon and/or Casale criteria) was observed in 296 (3.8%) patients. We examined the independent association between LVH (determined by the admission ECG) and outcomes in relation to STD. Patients with LVH were older, had more comorbidities and STD, and presented with a higher Killip class. They were less likely to undergo cardiac catheterization (43.1% vs 51.2%, P = .006) and percutaneous coronary intervention (18.3% vs 24.6%, P = .014). Patients with LVH had higher unadjusted mortality at 6 months (10.5% vs 7.1%, P = .038), but similar rates of in-hospital mortality (4.1% vs 3.4%, P = .54) and reinfarction (7.1% vs 7.6%, P = .75). Patients with LVH were more likely to have heart failure in-hospital (21.8% vs 11.8%, P < .001). Among LVH patients, degree of quantitative STD did not predict higher short- or long-term mortality, but was associated with in-hospital heart failure. Multivariable analysis adjusting for other clinical prognosticators of the GRACE risk models revealed that LVH was not a significant independent predictor of in-hospital mortality (adjusted odds ratio = 0.75, 95% CI 0.40-1.41, P = .37) or 6-month mortality (adjusted odds ratio = 0.83, 95% CI 0.52-1.35, P = .44). In contrast, STD remained a strong independent predictor of adverse outcomes. There was no significant interaction between STD and LVH. Across the broad spectrum of NSTE-ACS, LVH is associated with adverse prognostic factors including STD. Electrocardiographic-determined LVH provides no significant additional prognostic utility beyond comprehensive risk assessment using the GRACE risk score. The adverse prognosis associated with LVH in NSTE-ACS may be attributable to other prognosticators such as STD.

Particulate air pollution as a risk factor for ST-segment depression in patients with coronary artery disease.

The association of particulate matter (PM) with cardiovascular morbidity and mortality is well documented. PM-induced ischemia is considered a potential mechanism linking PM to adverse cardiovascular outcomes. In a repeated-measures study including 5979 observations on 48 patients 43 to 75 years of age, we investigated associations of ambient pollution with ST-segment level changes averaged over half-hour periods measured in the modified V(5) position by 24-hour Holter ECG monitoring. Each patient was observed up to 4 times within 1 year after a percutaneous intervention for myocardial infarction, acute coronary syndrome without infarction, or stable coronary artery disease without acute coronary syndrome. Elevation in fine particles (PM(2.5)) and black carbon levels predicted depression of half-hour-averaged ST-segment levels. An interquartile increase in the previous 24-hour mean black carbon level was associated with a 1.50-fold increased risk of ST-segment depression > or =0.1 mm (95% CI, 1.19 to 1.89) and a -0.031-mm (95% CI, -0.042 to -0.019) decrease in half-hour-averaged ST-segment level (continuous outcome). Effects were greatest within the first month after hospitalization and for patients with myocardial infarction during hospitalization or with diabetes. ST-segment depression is associated with increased exposure to PM(2.5) and black carbon in cardiac patients. The risk of pollution-associated ST-segment depression may be greatest in those with myocardial injury in the first month after the cardiac event.

Mechanisms of exercise‐induced ST‐segment depression in patients without typical angina pectoris

To evaluate if exercise-induced ST-segment depression without typical angina pectoris is related to increases in sympatho-adrenal activity or beta-adrenoceptor sensitivity. Thirteen patients (four men) aged 35-62 years with ST-segment depression during exercise but atypical symptoms and normal myocardial scintigraphy, and 13 matched controls. Patients and controls were compared regarding responses with: (i) exercise testing without treatment, (ii) exercise testing following beta-adrenoceptor blockade by propranolol (0.15 mg kg(-1) i.v.), (iii) incremental adrenaline infusions (0.1, 0.2, 0.4 and 0.8 nmol kg(-1) min(-1)) and (iv) adrenaline infusions during alpha-adrenoceptor blockade by phentolamine (0.5 mg min(-1)). ST-segment depression and tissue Doppler parameters reflecting contractility. Exercise lowered the ST-segment by 2.44 mm without and 0.87 mm with beta-adrenoceptor blockade (P < 0.001 for difference) amongst patients, but not amongst controls. Maximal heart rate was slightly higher amongst patients (P < 0.05), despite similar loads and plasma catecholamine responses to exercise in the two groups; this difference disappeared after beta-adrenoceptor blockade with propranolol. ST-segment depression during adrenaline infusion was greater in patients compared with controls (P < 0.01) despite similar increases in heart rate. alpha-Blockade enhanced the ST-segment depression (P < 0.001) and heart rate (P < 0.001) responses to adrenaline infusion more markedly amongst patients. Tissue Doppler imaging showed similar contractility and diastolic relaxation responses of patients and controls to adrenaline, but early diastolic movements did not increase amongst patients after phentolamine (P < 0.01). Exercise-induced ST-segment depression in patients with a low likelihood of ischaemic heart disease is related to increased beta-adrenergic sensitivity regarding chronotropic and electrophysiological, but not inotropic responses.

Effect of spinal cord stimulation on spontaneous and stress-induced angina and ‘ischemia-like’ ST-segment depression in patients with cardiac syndrome X

A significant number of patients with cardiac syndrome X (CSX) present frequent episodes of severe chest pain, refractory to maximal multi-drug therapy. A few, small, uncontrolled data suggested that spinal cord stimulation (SCS) may have favourable clinical benefits in these patients. We studied 10 CSX patients who were being treated by SCS for refractory angina pectoris for 17+/-16 months (median 8). Patients were randomized to either continue or withdraw SCS for a period of 3 weeks and were then crossed over to the other condition for a further 3-week period. During each 3-week period patients kept a detailed diary of angina episodes occurring in the last 2 weeks of each phase. Furthermore, at the end of each 3-week period, angina status was also assessed by Seattle Angina Questionnaire (SAQ), a 0-100 visual analogue scale (VAS), and patients underwent 24-h Holter monitoring (HM) and echocardiographic dobutamine stress test (DST). Compared with the withdrawal phase, SCS reduced the number (P=0.01), duration (P=0.022), and severity (P=0.011) of angina episodes, and nitrate consumption (P=0.042). SAQ scores (P< or =0.013 for all) and VAS (P<0.001) were also improved, the number of episodes of ST-segment depression on HM was decreased (P=0.014), and time to angina (P=0.045) and to 1 mm ST-segment depression (P=0.04) during DST were both prolonged by SCS. Our data point out that SCS may be an effective form of treatment in patients with CSX suffering from frequent angina episodes significantly impairing quality of life (QOL) and refractory to maximally tolerated drug therapy.

Prognostic value of the admission electrocardiogram in patients with unstable angina/non-ST-segment elevation myocardial infarction treated with very early revascularization

Study Question: The study goals were to determine if very early revascularization might ameliorate the adverse prognosis associated with ST-segment depression in patients with unstable angina/non-ST-segment elevation myocardial infarction (MI). Method: In this prospective cohort study, 1450 consecutive patients with unstable angina/non-ST-segment elevation MI were stratified by either the presence of ST-segment depression, T-wave inversion, or no changes on the admission electrocardiogram (ECG). All patients underwent coronary angiography and, if appropriate, revascularization within 24 h after admission. The primary end point of the study was all-cause mortality. Results: During up to 59 months of follow-up, the in-hospital mortality rate was 2.1% (19/895) in patients with no ECG changes, 4% (6/136) in those with ST-segment depression, and 0.2% (1/419) in those with no ECG changes, 19.9% (n=18) in at 36 months was 8.0% (n=49) in patients with no ECG changes, 19.9% (n=18) in patients with ST-segment depression, and 5.1% (n=13) in patients with T-wave inversion (p=0.0001 by log-rank). After adjustment for potential cofounders, ST-segment depression (hazard ratio [HR]=2.2; 95% confidence interval [CI]: 1.1–4.6) and T-wave inversion (HR=0.44; 95% CI: 0.20–0.96) were associated with long-term mortality. Conclusions: The researchers concluded that ST-segment depression and T-wave inversion on the admission ECG are important predictors of outcome in patients with unstable angina/non-ST-segment elevation MI and who are undergoing very early revascularization. Perspective: The study suggests that new ST-segment depression and new T-wave inversion on the admission ECG herald very different prognoses in patients with unstable angina/non-ST-segment elevation MI who undergo very early revascularization. In contrast to the considerable morbidity and mortality seen in patients with ST-segment depression, T-wave inversion appears to be associated with a more favorable outcome independent of potential cofounders, including gender. DM

Prognostic value of the admission electrocardiogram in patients with unstable angina/non–ST-segment elevation myocardial infarction treated with very early revascularization

Purpose The goals of this study were to determine if very early revascularization might ameliorate the adverse prognosis associated with ST-segment depression in patients with unstable angina/non–ST-segment elevation myocardial infarction. Methods In this prospective cohort study, 1450 consecutive patients with unstable angina/non–ST-segment elevation myocardial infarction were stratified by the presence of ST-segment depression, T-wave inversion, or no changes on the admission electrocardiogram (ECG). All patients underwent coronary angiography and, if appropriate, revascularization within 24 hours after admission. The primary endpoint was all-cause mortality. Results During up to 59 months of follow-up, the in-hospital mortality rate was 2.1% (19/895) in patients with no ECG changes, 4% (6/136) in those with ST-segment depression, and 0.2% (1/419) in those with T-wave inversion. The cumulative death rate at 36 months was 8.0% (n = 49) in patients with no ECG changes, 19.9% (n = 18) in patients with ST-segment depression, and 5.1% (n = 13) in patients with T-wave inversion ( P = 0.0001 by log-rank). After adjustment for potential cofounders, ST-segment depression (hazard ratio [HR] = 2.2; 95% confidence interval [CI]: 1.1 to 4.6) and T-wave inversion (HR = 0.44; 95% CI: 0.20 to 0.96) were associated with long-term mortality. Conclusion ST-segment depression and T-wave inversion on the admission ECG were important predictors of outcome in patients with unstable angina/non–ST-segment elevation myocardial infarction undergoing very early revascularization. In contrast to the considerable mortality seen in patients with ST-segment depression, T-wave inversion was associated with a more favorable outcome.

1094-160 Prognostic significance of dipyridamole-induced ST-segment depression in patients with normal rubidium-82 positron emission tomography perfusion images

1094-160 Prognostic significance of dipyridamole-induced ST-segment depression in patients with normal rubidium-82 positron emission tomography perfusion images

The electrocardiographic differential diagnosis of ST segment depression

The importance of the electrocardiographic differential diagnosis of ST segment depression in patients presenting with acute chest pain is discussed.

Long-term effects of the alpha, beta-blocker arotinolol on stable effort angina pectoris using 24-hour ambulatory electrocardiographic monitoring: an open-label, pilot study

Background: Beta-blockers are effective in patients with effort angina pectoris. However, there have been no previous reports on the long-term effects of beta-blocker therapy using ambulatory electrocardiographic (AECG) monitoring according to a MEDLINE ® search. Objective: This study was undertaken to assess the long-term effects of the alpha, beta-blocker arotinolol in patients with stable effort angina pectoris using AECG monitoring. Methods: This pilot study involved patients with Canadian Cardiovascular Society class I or II stable effort angina pectoris and left ventricular ejection fraction >40% assessed using 2-dimensional echocardiography in whom percutaneous transluminal coronary angioplasty and coronary artery bypass grafting had not been performed. Patients were excluded if they were >75 years of age, had congestive heart failure of New York Heart Association class III or IV, or had a confirmed diagnosis of an illness likely to shorten their life span (eg, cancer, cirrhosis). Effort angina pectoris was diagnosed based on chest pain on effort and myocardial ischemia as demonstrated by stress thallium-201 myocardial perfusion scintigraphy and significant ST-segment depression on exercise electrocardiogram. The alpha, beta-blocker arotinolol 20 mg/d, divided into 2 doses of 10 mg each, was administered orally for 2 years. Patients were seen by the same physician at 2-week intervals during the first 6 weeks of treatment and at 4-week intervals thereafter, at which times chest pain, nitrate consumption, blood pressure, and heart rate were assessed. AECG monitoring was performed before treatment, at 6 weeks, and after 2 years of treatment. Results: Results were assessable in 12 of 18 patients at 4 institutions (6 withdrew from the study within 4 weeks of treatment) with a mean (±SD) age of 65 ± 3 years. The number of episodes per day of chest pain decreased significantly ( P < 0.05) at 6 weeks and became rare 2 years after treatment. There was significant improvement ( P < 0.05) during the daytime at both 6 weeks and 2 years in the number of episodes (0.1 ± 0.4 and 0.1 ± 0.3, respectively, vs 0.9 ± 1.1) and the duration (3.8 ± 7.0 and 0.4 ± 1.6 minutes, respectively, vs 40.9 ± 27.8 minutes) of ST-segment depression. The incidence and duration of ST-segment depression decreased significantly ( P < 0.05) in the nighttime at 2 years compared with baseline (0.2 ± 0.04 and 0.04 ± 1.6 minutes vs 1.9 ± 0.9 and 23.9 ± 31.5 minutes, respectively). Daytime heart rate decreased significantly ( P < 0.05), from 84 ± 11 beats/min before treatment to 69 ± 12 beats/min at 6 weeks and 67 ± 12 beats/min at 2 years; nighttime heart rate also decreased significantly ( P < 0.05), from 70 ± 11 beats/min before treatment to 65 ± 9 beats/min at 6 weeks and 59 ± 7 beats/min at 2 years. Conclusions: Arotinolol improved the incidence and duration of ST-segment depression in patients with stable effort angina pectoris on AECG monitoring by decreasing heart rate. Because the improvement was more marked after 2 years than after 6 weeks, we concluded that arotinolol is beneficial in the long-term treatment of patients with stable effort angina pectoris, although a larger study using a control group is needed to confirm our results.

Exercise-induced ST-segment depression and systolic dysfunction in patients with nonobstructive hypertrophic cardiomyopathy

Background ST-segment depression is common in patients with hypertrophic cardiomyopathy (HCM). However, it is not clear whether exercise-induced ST-segment depression in patients with HCM and patent coronary arteries is associated with changes in left ventricular function. Methods Left ventricular function was continuously evaluated in 53 patients with nonobstructive HCM during supine ergometer exercise with a radionuclide ventricular function monitor equipped with a cadmium telluride detector. On the basis of the ST-segment changes during exercise, the patients were divided into 2 groups: group N had no ST-segment depression, and group D had ≥0.1 mV ST-segment depression. Results Exercise duration, blood pressure, heart rate, and rate-pressure product during exercise did not differ between the 2 groups. End-diastolic volume at rest and at peak exercise did not differ between groups D and N. In contrast, the end-systolic volume in group N decreased during exercise, whereas in group D it increased. As a result, the left ventricular ejection fraction in group D decreased from 70% ± 7% to 59% ± 15% (P <.0001), whereas ejection fraction in group N increased from 65% ± 8% to 71% ± 11% (P =.0002). There was a strong correlation between exercise-induced ST-segment depression and changes in ejection fraction from rest to peak exercise (P <.0001). Conclusions These results suggest that the exercise-induced ST-segment depression seen in patients with nonobstructive HCM is associated with systolic dysfunction during exercise. (Am Heart J 2000;140:52-60.)

The significance of stress-induced ST segment depression in patients with inferior Q wave myocardial infarction

OBJECTIVESThis study was conducted to evaluate the relationship between ST segment depression (STD) during dobutamine stress tests in different electrocardiogram (ECG) leads and myocardial ischemia assessed by simultaneous single photon emission computed tomography (SPECT) imaging in patients with inferior Q wave myocardial infarction.BACKGROUNDSTD is a standard electrocardiographic sign of myocardial ischemia. Although STD may represent reciprocal changes in patients with previous myocardial infarction, studies of reciprocal changes during stress tests are scarce.METHODSDobutamine (up to 40 μg/kg/min) stress and rest myocardial perfusion scintigraphy using technetium SPECT imaging was performed in 125 patients >3 months after Q wave inferior myocardial infarction. The location of STD at the ECG was defined as anterior (V1–4), high lateral (I, aVL) and lateral (V5,6). Ischemia was defined as reversible perfusion abnormalities.RESULTSSTD occurred in the high lateral leads in 20 patients, in the anterior leads in 12 patients and in the lateral leads in 2 patients. ST segment elevation occurred in 25 patients in the inferior leads. High lateral STD was associated with inferior ST elevation in 16 patients (80%). There was a significant inverse linear correlation between the magnitude of ST segment shift from rest to peak stress in the inferior and the high lateral leads (r = −0.8, p < 0.0005), whereas no significant correlation was found between ST segment shift in the inferior and the anterior leads (r = −0.1, p = NS) or between the inferior and the lateral leads (r = 0.15, p = NS). Ischemia was detected in 45% of patients with and in 42% of patients without high lateral STD (p = NS). Patients with high lateral STD had a higher prevalence of fixed perfusion defects in the inferior wall (100% vs. 70%) and in the posterolateral wall (55% vs. 29%) compared with other patients (both p < 0.05). Ischemia was more prevalent in patients with anterior STD than without (75% vs. 39%, p < 0.05).CONCLUSIONSIn patients with inferior Q wave myocardial infarction, stress-induced STD in high lateral leads should be recognized as a reciprocal change for ST elevation in the inferior leads, and therefore, should be interpreted with the consideration of the significance of ST elevation if present, rather than being indicative of myocardial ischemia on its own. The STD found in the anterior leads appears to be a sign of myocardial ischemia. These findings should be considered in the definition of a positive ECG stress test and in establishing the criteria for the termination of stress test.

Comparison of coronary endothelial dynamics with electrocardiographic and left ventricular contractile responses to stress in the absence of coronary artery disease

Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 μg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 μg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5 ± 13% vs +1 ± 13%, p = 0.386) and flow (+179 ± 90% vs +169 ± 96%, p = 0.756), or in the systolic wall thickening responses (+134 ± 65% vs +118 ± 57%, p = 0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121 ± 73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129 ± 48%, p = 0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.

Hemodynamic Determinants of Silent ST Segment Depression in Patients with Hypertrophic Cardiomyopathy Treated with Verapamil

Objective: The aim of the study was to establish mechanisms of ischemic type, painless ST segment depression in nine patients with nonobstructive hypertrophic cardiomyopathy (HC) treated effectively by verapamil.Methods: Simultaneous 24‐hour Holter and blood pressure monitoring (measurements every 15 minutes) was performed to determine approximate indices of myocardial oxygen demand (double product), myocardial oxygen supply (diastolic blood pressure), and ST segment level during each minute when blood pressure measurements were obtained. According to ST segment level, all recordings were divided into four subgroups (one without and three with gradually increasing magnitude of ST segment depression) in which average double product and diastolic blood pressure were calculated.Results: Increasing ST segment depression coincided with gradual rises in double product indicating increasing myocardial oxygen consumption. Diastolic blood pressure was low in the group without ST segment deviation whereas it was significantly higher only in groups with ST segment depression of more than 2 mm.Conclusion: Verapamil‐induced, excessive fail of diastolic blood pressure was not associated with exacerbating ST segment depression. On the other hand, occasionally verapamil insufficiently prevented increases of double product, which coincided with the prescence of painless ST segment depression episodes.

Determinants of exercise-induced ST segment depression in patients with coronary artery disease: a multivariate approach.

The purpose of this study was to delineate among the usually gathered parameters in an electrocardiographic exercise test the determinants of its positive outcome (delta ST decreases > or = 1 mm measured at 80 msec from the J point). The authors studied 832 patients investigated with Bruce's exercise testing and with diagnostic coronary arteriography, all of whom were shown to have significant coronary artery disease (diameter stenosis > or = 50%). Twenty-five demographic, clinical, electrocardiographic, exercise, and anatomic/hemodynamic parameters were analyzed. The stepwise forward logistic regression analysis retained seven among them as significant independent predictors: four as positive contributors: (1) three-vessel and/or left main disease (P = 0.0000), (2) Gensini's angio-graphic score for disease extent (P = 0.0025), (3) anginal pain during the test (P = 0.0000), and (4) age (P = 0.0031) and three as negative contributors: (1) resting heart rate (P = 0.0004), (2) history of old myocardial infarction (P = 0.0019), and (3) pathological Q waves at the resting ECG (P = 0.0018). These findings establish standards that permit the prediction of the positive electrocardiographic exercise outcome in patients with significant coronary disease.

Ischemic-like ST-Segment Changes During Holter Monitoring in Patients With Angina Pectoris and Normal Coronary Arteries But Negative Exercise Testing

To evalutate whether Holter electrocardiographic monitoring may improve the detection of ST-segment depression in patients with anginal chest pain and normal coronary arteries, we performed symptom-limited exercise testing and 24-hour Holter monitoring in a group of 38 such patients (27 women, age 54 ± 8 years). Patients were divided into 2 groups: group X1 included 28 patients with and group X2 10 patients without significant ST-segment depression during exercise testing. There were no significant differences between the 2 groups in age, gender, characteristics of chest pain, exercise duration, heart rate (HR), and blood pressure at peak exercise, but anginal pain during exercise testing was reported by 10 patients of group X1 (36%) and 9 of group X2 (90%) (p <0.01). Episodes of ST-segment depression on Holter monitoring were found in 17 patients of group X1 (61%) and in 5 patients of group X2 (50%) (p = NS). There were no differences between the 2 groups in daily number of ST episodes (3.6 ± 4 vs 2.8 ± 5 episodes per patient), symptomatic episodes (8% vs 18%), and duration of the episodes. On average, HR increased significantly, in a similar way, from 15 minutes before ST-segment depression to 1-mm ST in both groups, and its value at the onset of ischemia was similar in the 2 groups (102 ± 22 vs 109 ± 18 beats/min, p = NS). Finally, HR at 1-mm ST during Holter monitoring was significantly lower than that observed at 1-mm ST during exercise testing (127 ± 16 beats/min, p ≤0.01) in group X1, and it was also lower than that observed at peak exercise (136 ± 22 beats/min, p ≤0.01) in group X2. In conclusion, Holter monitoring can significantly increase the detection of ST-segment depression in patients with anginal pain and normal coronary arteries, indicating a cardiac, although not necessarily ischemic, origin of the pain. Indeed, 50% of our patients with negative symptom-limited exercise testing showed spontaneous ST changes, compatible with transient myocardial ischemia, during daily activities. Differences in the response of coronary microvascular tone to exercise testing and to stimuli operating during daily life are likely to play a significant role in determining these findings.