Electrocardiographic ST Depression Research Articles

A case report of dipyridamole stress-induced ST depression progressing to ST-elevation myocardial infarction despite intravenous aminophylline: steal, spasm, or something else?

BackgroundDipyridamole stress is commonly used for myocardial perfusion imaging and is generally safe. Myocardial ischaemia can occasionally occur and is classically thought to be due to coronary steal as a result of redistribution of flow away from collateral dependent myocardium. Although ischaemia more commonly presents as electrocardiographic (ECG) ST depression and angina, ST-elevation myocardial infarction may occur as a very rare complication.Case summaryWe report a case of a patient who developed chest pain and ST depression during dipyridamole infusion. The pain persisted despite intravenous aminophylline with new inferior ST elevation soon after. Coronary angiography showed subtotal right coronary artery occlusion with no collateral supply. The symptoms and ECG changes resolved after percutaneous coronary intervention.DiscussionCoronary steal may not fully account for our patient’s presentation given the failure of aminophylline and absent angiographic collaterals. Vasospasm may be triggered by dipyridamole and can directly cause ischaemia or provoke rupture of an unstable plaque. Augmentation of cardiac energetics during vasodilator stress may also play a role.

Mortality and cardiovascular morbidity among long‐term endurance male cross country skiers followed for 28–30 years

Longevity and reduced mortality and cardiovascular disease (CVD) mortality and morbidity compared with the general population are described among former athletes in a few studies only. The aim of the study was to assess the outcomes of mortality and CVD morbidity after 30 years follow-up in long-term cross country skiers. The study was based on three different age groups of 122 long-term long-endurance cross country skiers participating in studies in 1976 and 1981. A total of 78/85 skiers completed the 28-30 year follow-up, while 37 were dead. Causes of deaths through 2006 were ascertained using the National Death Register. Morbidity or mortality data were available in 115 subjects. Total deaths were 31% compared with 40% in the general male population (P=0.04). Exercise electrocardiographic ST-depression in 1981 was associated with the later appearance of coronary heart disease (HR 2.90; P=0.033). Body mass index and average systolic blood pressure from 1976 to 1981 were predictors of later appearance of CVD (HR 1.23; P=0.034 and HR 1.03; P=0.048, respectively). Long-term aerobic exercise appears to be associated with reduced all-cause mortality.

Usefulness of Quantitative Assessment of Electrocardiographic ST Depression for Predicting New-Onset Heart Failure in American Indians (from the Strong Heart Study)

The qualitative electrocardiographic strain pattern of ST depression (STD) and T-wave inversion is strongly associated with coronary heart disease and left ventricular hypertrophy and is an independent predictor of new-onset heart failure in hypertensive participants. However, whether quantitative measures of STD in the lateral precordial leads predict new heart failure is unclear. Digital electrocardiograms were examined in 2,059 American-Indian participants in the second Strong Heart Study examination with no history of heart failure. The absolute magnitude of ST segment deviation was measured using computer to the nearest 5 microV in leads V(5) and V(6). During 5.7 +/-1.4 years of follow-up, heart failure developed in 77 participants (3.7%). Participants who developed heart failure had greater STD in leads V(5) or V(6) (-11 +/- 35 vs 12 +/- 27 microV; p <0.001) than those who did not. In univariate Cox analyses, STD was a significant predictor of new heart failure, with each 10-microV greater STD associated with a 31% greater risk of heart failure (hazard ratio [HR] 1.31, 95% confidence interval [CI] 1.24 to 1.39). Increasing STD grouped according to quartiles was strongly associated with the development of heart failure, with stepwise increasing risk of heart failure compared with the lowest quartile of STD for the second (HR 2.39, 95% CI 0.77 to 7.40), third (HR 3.01, 95% CI 1.00 to 9.08), and fourth quartiles of STD (HR 9.06, 95% CI 3.26 to 25.16). In Cox multivariate analyses controlling for age, gender, diabetes, coronary heart disease, albuminuria, and other baseline risk factors, STD remained a significant predictor of incident heart failure (HR 1.22, 95% CI 1.13 to 1.32 per 10-muV increment in STD; p <0.001). In conclusion, increasing STD in lateral precordial leads is strongly associated with increased risk of developing heart failure independent of other risk factors for new heart failure.

Combined echocardiographic left ventricular hypertrophy and electrocardiographic ST depression improve prediction of mortality in American Indians: the Strong Heart Study.

Echocardiographic left ventricular hypertrophy (Echo-LVH) and ST segment depression (STD) on the ECG have each been demonstrated to predict cardiovascular (CV) and all-cause (AC) mortality. However, the prognostic value of combining Echo-LVH and ECG-STD has not been examined. ECGs and echocardiograms were examined in 2193 American Indian participants in the second Strong Heart Study examination. STD was measured by computer and was considered abnormal if > or =50 microV. Echo-LVH was defined by indexed LV mass >116 g/m2 in men and >104 g/m2 in women. After a mean follow-up of 3.1+/-0.7 years, there were 57 CV and 169 AC deaths. In univariate Cox analyses, Echo-LVH (chi2=54.2 and chi2=68.5) and ECG-STD (chi2=35.9 and chi2=46.3, all P<0.001) predicted CV and AC mortality, respectively. The combination of Echo-LVH and ECG-STD improved risk stratification compared with either alone for both CV death (chi2=74.4, P<0.001) and AC death (chi2=102.0, P<0.001), with presence of both ECG-STD and Echo-LVH associated with the greatest risks. After adjustment for age, sex, and relevant risk factors, combined Echo-LVH and ECG-STD remained predictive of CV mortality (chi2=19.7, P<0.001) and AC mortality (chi2=24.9, P<0.001), with the presence of both Echo-LVH and ECG-STD associated with a 6.3-fold increased risk of CV death (95% CI: 2.8 to 14.2) and a 4.6-fold increased risk of AC mortality (95% CI: 2.5 to 8.5). ECG-STD and Echo-LVH additively increase the risk of both CV mortality and AC mortality. These findings support the value of combining Echo-LVH and ECG-STD to improve risk stratification. These findings require verification in other populations.

Electrocardiographic ST segment depression and clinical function in children with Fontan circulation.

Previous studies noted that Fontan patients have electrocardiographic ST depressions during exercise tests and on 24-hour ambulatory electrocardiographic (ECG) monitoring. This study investigated whether the ST depressions were correlated to clinical function (NYHA Functional Classification). Forty-five children in two groups were examined--15 patients with Fontan circulation and 30 with a structurally normal heart, matched for sex, height, and weight. Clinical and echocardiographic examinations were performed. The clinical state was defined as NYHA functional classes I-IV. All 45 children underwent 24-hour ECG and an analysis of ST changes was performed, with ST segment depression > 0.20 mV at ST 60 regarded as significant. Twelve of 15 patients had significant 24-hour ECG ST depressions; in 9 of 12 patients these occurred on more than one occasion. Comparing 24-hour ECG recordings from patients in NYHA I with patients in NYHA II or III showed a significant difference in depth (p = 0.0023), duration (p = 0.0016), and number of ST depressions (p = 0.0001). None of the matched healthy children showed ST depressions. Repeated ST analysis on 24-hour ECG shows that the ST depressions seem to be correlated to functional status and this may be a useful tool in clinical praxis.

Release of cardiac troponin I after temporally graded acute coronary ischaemia with electrocardiographic ST depression

Background: Elevation of cardiac biochemical markers and ST segment depression in the electrocardiogram have important roles in the risk stratification of unstable coronary syndromes. We assessed graded duration of acute coronary ischaemia with ST depression versus release of cardiac troponin I (cTnI) and conventional cardiac markers in 15 ischaemic pigs and 11 controls. Methods: Coronary ischaemia was induced via percutaneous technique by semiinflating an angioplasty balloon in the left circumflex artery. Blood velocity monitored by Doppler was reduced until ST depression ≥0.1 mV was obtained. Among 26 pigs, six controls had jugular vein sheath introduced only, five controls jugular vein and bilateral femoral sheaths, and 15 pigs were divided into three equal groups ( n=5) in which ischaemia was maintained for 10, 20 and 30 min, respectively. Results: Mean blood flow velocity (cm/s) at baseline was 16.3±6.5 and was reduced to 4.1±3.2 (25% of normal, range 20-29%) during ischaemia. cTnI (μg/l) did not increase in controls but increased from 0.05 to 0.52 ( P<0.05) and 0.76 ( P<0.05) with 10 and 20 min of ischaemia, and to 30.77 ( P<0.05) with 30 min of ischaemia. A rise of myoglobin and conventional cardiac enzymes did not distinguish controls with arterial cut-down from the ischaemia groups. Conclusion: Release of cTnI depends on the duration of ST depression ischaemia. The critical time for a major release seems to be between 20 and 30 min. Thus, very early intervention in patients with prolonged ST depression ischemia should be focused on in future clinical trials.

Current guidelines for the management of unstable angina: a new diagnostic and management paradigm*

The new guidelines reflect a worldwide change to more sensitive diagnostic strategies and more aggressive management of unstable angina. Stratification to high risk now includes those patients with only a minor degree of electrocardiographic ST depression (0.5 mm) or a significant elevation of cardiac troponin. High-risk patients are recommended to be treated with intensive medical and invasive management. Intermediate-risk patients may be best evaluated using an accelerated diagnostic strategy over an 8-12 h period before being reclassified as high or low risk.

Current guidelines for the management of unstable angina: a new diagnostic and management paradigm*

The new guidelines reflect a worldwide change to more sensitive diagnostic strategies and more aggressive management of unstable angina. Stratification to high risk now includes those patients with only a minor degree of electrocardiographic ST depression (0.5 mm) or a significant elevation of cardiac troponin. High-risk patients are recommended to be treated with intensive medical and invasive management. Intermediate-risk patients may be best evaluated using an accelerated diagnostic strategy over an 8–12 h period before being reclassified as high or low risk. (Intern Med J 2001; 31: 104–111)

Electrocardiographic ST-segment depression in children with fontan circulation.

Despite successful operation, many patients palliated with a Fontan-type procedure continue to show effort limitation. We previously observed that these children showed electrocardiographic ST depression during exercise tests. The purpose of the study was to investigate whether electrocardiographic ST depression is a common finding in children with Fontan circulation. Forty-two children in two groups were examined: group A consisted of 14 patients who had all undergone a modified Fontan procedure, and group B consisted of 28 children with a structurally normal heart, matched for length, weight and gender to group A. Complete echocardiographic examinations were performed in all patients and controls. All 14 patients and all 28 healthy children underwent standard 24 h ambulatory electrocardiographic monitoring. All the recordings were analysed by a PC-based Holter system where an analysis of ST changes was performed. Seven patients and 14 matched healthy children were exercised on bicycle ergometers. Four patients and eight matched healthy children underwent exercise testing by walking/running a treadmill. Ten of 13 patients analysed had significant ST depressions on ambulatory electrocardiogram (>0.20 mV). Three of the 10 patients with ST depression were on digoxin. Three patients showed depressions of the ST segment in the electrocardiogram during exercise, with a maximal depression of 0.20-0.35 mV. None of the 28 matched healthy children showed electrocardiographic ST depression on the ambulatory 24 h ECG. These findings indicate that ST depression in daily activity is a common finding in children with Fontan circulation.

Epicardial ST depression in acute myocardial infarction.

The presence of electrocardiographic ST depression in acute infarction remains controversial and poorly explained. A combined animal and modeling study was performed to evaluate the source of ST changes in acute infarction. In anaesthetized sheep, small infarcts showed uniform ST elevation over the infarction whereas larger infarcts showed marked ST depression over the normal myocardium in addition to the ST elevation. These findings were replicated by bidomain models of the heart. A hollow sphere was used to model a gradually increasing infarct, and this showed that there was a decrease in the ratio of ST elevation to ST depression as the infarct was increased. The current flowing out of the heart must be identical to the current flowing back into the heart. This means that any infarction will produce ST depression as well as ST elevation, the ratio between the two being related to the size of the infarction. Small infarction is associated with a small region of ST elevation and minor ST depression of the remaining myocardium, and as the infarct region increases, the amplitude of the epicardial ST elevation falls and the amplitude of the ST depression increases. Infarction size is proportional to both the height of the ST depression on the epicardium and the strength of the epicardial ST segment dipole.

Relation between the electrocardiographic stress test and degree and location of myocardial ischemia

Factors that influence frequency and location of stress-induced electrocardiographic (ECG) ST depression and the development of chest pain are incompletely understood. We studied 331 patients with ischemic myocardial nuclear defects in response to routine clinical treadmill testing with simultaneous ECG recording. Nuclear defects were analyzed for location and extent of myocardium involved. Exercise-induced ischemic ST changes were demonstrated in 59% of patients (196 of 331). Subjects with stress-induced ECG changes and/or chest pain had more extensive nuclear perfusion defects. Diabetic patients were significantly less likely to experience chest pain (24%) versus nondiabetics (41%) during testing (p = 0.04). Larger perfusion defects were associated with greater magnitude, lead distribution, and incidence of ECG changes. The number of ECG lead zones (anterior, lateral, and inferior) responding positively were related to both magnitude of ST depression and severity of ischemia, but not to location of ischemic defects. Regardless of location of ischemia, ST depression occurred with similar frequency. Thus, exercise-induced ECG ST depression remains a valuable indicator of the severity of myocardial ischemia. Greater ST depression involving multiple leads usually signified extensive myocardial ischemia, but provided no information regarding its location. Anginal-type chest pain induced by exercise testing also denoted more extensive ischemia.

Source of electrocardiographic ST changes in subendocardial ischemia.

To clarify the source of electrocardiographic ST depression associated with ischemia, a sheep model of subendocardial ischemia was developed in which simultaneous epicardial and endocardial ST potentials were mapped, and a computer model using the bidomain technique was developed to explain the results. To produce ischemia in different territories of the myocardium in the same animal, the left anterior descending coronary artery and left circumflex coronary artery were partially constricted in sequence. Results from 36 sheep and the computer simulation are reported. The distributions of epicardial potentials from either ischemic source were very similar (r=0.77+/-0.14, P<0.0001), with both showing ST depression on the free wall of the left ventricle and no association between the ST depression and the ischemic region. However, endocardial potentials showed that ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial ST potentials, which was consistent with an intramyocardial source. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischemic center as ischemia became transmural. Computer simulation using the bidomain model reproduced the epicardial ST patterns and suggested that the ST depression was generated at the lateral boundary between ischemic and normal territories. ST depression on the epicardium reflected the position of this lateral boundary. The boundaries of ischemic territories are shared, and only those appearing on the free wall contribute to external ST potential fields. These effects explain why body surface ST depression does not localize cardiac ischemia in humans.

Ability of the exercise electrocardiogram test to detect ischemia in stable coronary artery disease patients with ST-segment depression on the resting electrocardiogram

Background The appearance of ST-segment depression on the exercise electrocardiogram (ETT) generally indicates myocardial ischemia. Disorders that produce ST-segment depression on the resting electrocardiogram can confound the results of the ETT. The purpose of this study was to assess the reliability of exercise ST-segment depression as an indicator of ischemia in patients with a resting electrocardiographic ST depression, presumably caused by coronary disease. Methods We studied 882 patients 1 to 6 months after a hospitalization for myocardial infarction or unstable angina as part of the Multicenter Study of Myocardial Ischemia. An ETT and thallium-201 perfusion scan were performed in all patients. For the purpose of this study, the perfusion scan was considered the “gold standard” for ischemia. We correlated the ETT ST-segment responses with the perfusion scan in a group with a normal electrocardiogram baseline ST segment (NO ST DEP group) and in a group with resting electrocardiographic ST depression ≥0.5 mm (ST DEP group). Results Although the frequency of ischemia by perfusion scan was similar in the ST DEP group (48%) to that in the NO ST DEP group (40%), the ST DEP group had a significantly higher (p = 0.03) sensitivity (54%) in detecting ischemia than the NO ST DEP group (35%). The ST DEP group, however, had a lower (58% vs 74%) specificity than the NO ST DEP group (p = 0.056). Baseline characteristics of the two groups probably account for these differences. The overall diagnostic accuracy is similar (58% vs 56%) in the two groups. Conclusion We conclude that in a stable population with known coronary disease, the presence of ST depression on the resting electrocardiogram does not impair the detection of ischemia by the ETT, but may be associated with a higher false-positive rate.(Am Heart J 1998;135:901-6.)

Effects of propranolol in patients entered in the Beta-Blocker Heart Attack Trial with their first myocardial infarction and persistent electrocardiographic ST-segment depression

Objective/Background It has been shown that patients with an acute myocardial infarction and persistent electrocardiographic ST-segment depression are at high risk for subsequent cardiac events. The purpose of this retrospective analysis was to examine the long-term effects of propranolol therapy in patients with their first acute myocardial infarction and persistent electrocardiographic ST-segment depression. Methods The outcomes of 2877 patients enrolled in the Beta-Blocker Heart Attack Trial (BHAT) with their first myocardial infarction (75% of patients in BHAT) were reviewed. Patients were divided into three groups on the basis of presence or absence of ≥1 mm ST-segment depression in two contiguous leads of the 12-lead electrocardiogram obtained soon after admission or at the time of randomization, which occurred 10.1 ± 3.5 days after the index myocardial infarction. Group 1 included 774 patients (392 randomly assigned to placebo and 382 to propranolol) with no ST-segment depression; group 2 included 1447 patients (713 placebo, 734 propranolol) with ST-segment depression at admission or at the time of randomization (labeled as transient); and group 3 included 656 patients (339 placebo and 317 propranolol) who had electrocardiographic ST-segment depression from the time of admission to the time of randomization (labeled as persistent). Results In group 3, patients with persistent electrocardiographic ST depression, the mortality rate in patients randomly assigned to placebo was 13.6% compared with 7.6% in patients with propranolol ( p = 0.012; log rank test). Sudden death in the placebo arm was 9.7% compared with 4.7% in the propranolol group ( p = 0.012, log rank test). The results of the Cox regression analysis, adjusting for all baseline variables with p values <0.25, showed the relative risk of overall mortality rate and the relative risk of sudden death were 2.13 (1.22, 3.70) and 2.56 (1.27, 5.26), respectively, for the placebo group compared with the propranolol group. Patients with persistent ST-segment depression had the greatest benefit from propranolol (47.2 fewer events [deaths/reinfarctions] per 1000 person-years compared with 7.8 and 2.1 fewer events in patients with transient and no ST-segment depression, respectively). Conclusions It appears that the greatest benefit for β-blocker therapy in patients after myocardial infarction is observed in patients with persistent ST-segment depression who are at greatest risk for death and reinfarction. Definitive conclusions regarding therapy with β-adrenergic blocking agents in patients with persistent ST-segment depression cannot be made because our analysis, given its retrospective nature, is only hypothesis generating. (Am Heart J 1998;135:261-7.)

The appearance of gallop rhythm after exercise stress testing.

Although it is generally assumed that the appearance of an early diastolic gallop, or third heart sound, appearing immediately after exercise during treadmill stress testing, indicates the presence of serious myocardial disease, no systemically collected data are available to test this hypothesis. The author performed auscultation on 3,679 patients undergoing routine treadmill testing together with thallium-201 perfusion scans. Exercise-induced diastolic sounds were related to the available clinical information and electrocardiographic and nuclear test results. These findings were compared with those of 665 randomly selected patients undergoing stress testing in whom such sounds were absent. A total of 165 patients had audible third heart sounds (Group 1). In comparison with those patients lacking such sounds (Group 2), there was a considerably greater prevalence of myocardial scarring (68.5 vs. 26.9%), abnormal lung uptake of thallium (40 vs. 12.8%), diabetes mellitus (20.6 vs. 6.2%), and left bundle-branch block on the resting electrocardiogram (ECG) (15.1 vs. 1.2%). In addition, 65 patients (39.3%) had dilatation of the left ventricle after exercise; 31 (18.8%) of these were also dilated at rest, but only 2 (1.2%) had a drop in blood pressure during stress. In those individuals also subjected to nuclear ventriculography, the average resting ejection fraction was 35%. Estimated exercise capacity was generally reduced in Group 1 (average peak of 6.6 METs), but 29 (17.6%) exceeded 9 METs. Sensitivity and specificity of electrocardiographic ST depression were relatively poor in the detection of perfusion defects within this group (36 and 62%, respectively). Of the 39 patients in Group 1 with a normal resting ECG, 19 (48.7%) had scar (usually posterior or lateral) on nuclear scans. In an additional 10 of this group, nuclear evidence of ischemia (often extensive) was found. An early or mid-diastolic gallop sound developing after exercise virtually always signifies myocardial disease with reduced myocardial function. Common associated findings are prior infarction (with or without associated ischemia), diabetes, and left bundle-branch block. When found in the presence of a normal resting ECG, this sound commonly signals the presence an occult left ventricular scar and, less commonly, extensive myocardial ischemia. In those patients manifesting such sounds, electrocardiographic ST changes in response to exercise appear limited in the detection of coronary ischemia.

Acute changes in atrial natriuretic peptide, insulin-like growth factor-1, and lactate levels during left anterior descending coronary artery angioplasty

This study examines acute changes in circulating levels of atrial natriuretic peptide (ANP) and insulin-like growth factor (IGF-1) during short periods of myocardial ischemia experienced at coronary angioplasty. Ten patients (mean age 55.7 ± 3.9 years, nine men) undergoing angioplasty to the left anterior descending coronary artery were studied. Angioplasty of the left anterior descending coronary artery was performed with the balloon inflations maintained at 6 to 10 atm for 20 to 90 seconds. Blood was sampled from the coronary sinus for ANP, IGF-1 (both total and free), and lactate levels at (1) after catheterization of the coronary sinus, (2) after the initial left coronary angiography, (3) immediately after balloon deflation, and (4) 5 minutes after deflation. ANP levels (pmol/L ± SEM) rose significantly at the end of balloon deflation (13.4 ± 2.8; p < 0.01) compared with baseline levels (8.8 ± 1.9). This rise was sustained for at least 5 minutes after balloon deflation (13.7 ± 3.1; p < 0.01). ANP levels were not affected by the injections of angiographic contrast media. Free IGF-1 levels rose after injections of radiographic contrast but not after balloon inflation or deflation. Total IGF-1 levels did not change significantly at any of the sampling times. Lactic acid (mmol/L) levels rose at the end of balloon inflation (2.66 ± 0.6) compared with baseline (2.13 ± 0.7; p < 0.05) but returned to normal within 5 minutes of balloon deflation. Neither lactic acid levels nor release of ANP or IGF-1 correlated with the initial left ventricular end-diastolic pressure or the degree of electrocardiographic ST depression during the procedure. Three patients had clinical and angiographic restenosis within 6 months of the angioplasty. These patients had higher levels of IGF-1 and greater IGF-1 release with injection of contrast media. We conclude that regional myocardial ischemia results in release of ANP from the myocardium and a transient increase in lactate concentrations. Total IGF-1 levels do not appear to be altered by ischemia, but this peptide appears to be displaced from the transporter protein by radiographic imaging media. IGF-1 may be a factor in the development of restenosis after angioplasty.

ST-segment depression and mortality after myocardial infarction

Source Citation Gheorghiade M, Shivkumar K, Schultz L, et al. Prognostic significance of electrocardiographic persistent ST depression in patients with their first myocardial infarction in the plac...

Prognostic significance of electrocardiographic persistent ST depression in patients with their first myocardial infarction in the placebo arm of the Beta-Blocker Heart Attack Trial

The prognostic significance of ST segment depression in patients with their first acute myocardial infarction was investigated in 1444 patients with an acute myocardial infarction, who were randomly assigned to the placebo arm of the Beta-Blocker Heart Attack Trial (BHAT). Patients were divided retrospectively into three groups based on the presence or absence of ≥1 mm ST segment depression in two contiguous leads of a 12-lead electrocardiogram obtained during the first few days after admission and at the time of randomization, which occurred at 9.7 ± 3.3 days after the index myocardial infarction. Group 1 included 392 patients with no ST segment depression, group 2 comprised 713 patients with transient ST segment depression in the first few days after admission or at the time of randomization, and group 3 included 339 patients with persistent ST segment depression in the first few days after admission and at the time of randomization. At a median follow-up of 26 months, the mortality rate was 4.9% in group 1, 7.6% in group 2, and 13.6% in group 3. When Cox regression was used to adjust for baseline differences in other variables, the differences between the three groups continued to be highly significant ( p = 0.005; 95% confidence intervals [0.6 and 1.4]). We conclude that persistent and transient ST segment depression in patients with their first myocardial infarction are strong predictors of increased long-term mortality when compared to patients without ST segment depression. These findings should be taken into consideration when stratifying patients at risk in the post-myocardial infarction period.

Effect of Transient Myocardial Ischemia on the Transmitral Blood Flow Profile

To evaluate the effect of transient myocardial ischemia on the transmitral blood flow profile, pulsed Doppler echocardiography was performed in 10 anesthetized dogs during brief occlusion of the coronary artery and in 79 patients with coronary artery disease (CAD) and 19 control subjects who underwent esophageal pacing or dipyridamole stress tests. During coronary artery occlusion, the peak velocity of the rapid filling wave (R) was rapidly reduced and that of atrial contraction (A) augmented. These changes of overall left ventricular diastolic filling variables surprisingly coincided with rapid deterioration of systolic wall thickening at the ischemic segment. In the clinical study, the transmitral flow profile did not change in controls during esophageal pacing. We observed similar changes in the transmitral flow profile in the experimental study in CAD patients. The deceleration time of the early diastolic filling wave was not changed in controls, but was significantly prolonged in CAD patients. Preadministration of sublingual nitroglycerin normalized the postpacing responses of peak velocities and deceleration times induced in CAD patients. With intravenous administration of 0.56 mg/kg of dipyridamole R and A increased, but the A/R ratio was unchanged in both controls and CAD patients. The deceleration halftime, however, was prolonged in CAD patients, as shown during esophageal pacing. These changes of transmitral flow patterns were transient and recovered within a few minutes. Furthermore, they were noted more frequently than the development of chest pain or electrocardiographic ST depression. However, induced changes of transmitral flow profile were not significantly different between patients with multivessel disease and those with single-vessel disease in both stress tests, so that there were limitations in diagnosing the extent of coronary artery disease. These findings suggest that peak velocities or deceleration time responses in transmitral blood flow are early and sensitive markers for evaluating abnormal left ventricular diastolic filling during transient myocardial ischemia. This noninvasive technique may be a reasonable alternative to other imaging examinations for detection and functional assessment of patients with CAD.

Hemodynamic and antianginal effects during rest and exercise of intravenous isradipine, a new dihydropyridine calcium antagonist

In an open randomized study, hemodynamic and antianginal effects of nifedipine and the new dihydropyridine derivative isradipine were compared in patients with stable, angiographically confirmed coronary heart disease. Right heart hemodynamics, systemic arterial blood pressure, ECG, and drug plasma concentrations were measured before medication at rest and exercise, after infusions of increasing doses at rest, and again after treatment at rest and exercise. A linear relationship between serum concentrations and cumulated dosages was obtained for both drugs. At rest, both drugs significantly increased cardiac output and heart rate. The reduction of arterial blood pressure was significantly greater after isradipine (systolic from 148 +/- 3 to 104 +/- 3 mmHg; diastolic from 90 +/- 4 to 58 +/- 2 mmHg) than after nifedipine (systolic 149 +/- 6 to 125 +/- 4 mmHg; diastolic 92 +/- 4 to 76 +/- 3 mmHg). The minimal effective plasma level of isradipine regarding blood pressure reduction was estimated at 5 ng/ml (nifedipine: 10-25 ng/ml). During exercise both medications significantly reduced mean pulmonary artery pressure (isradipine: 40 +/- 3 to 20 +/- 1 mmHg, nifedipine: 37 +/- 4 to 22 +/- 1 mmHg), pulmonary artery wedge pressure (isradipine: 23 +/- 3 to 10 +/- 1 mmHg, nifedipine 24 +/- 3 to 14 +/- 1 mmHg), and diastolic arterial pressure (isradipine: 103 +/- 3 to 73 +/- 4 mmHg, nifedipine: 99 +/- 3 to 91 +/- 2 mmHg), whereas systolic pressure was reduced by only isradipine (189 +/- 4 to 147 +/- 5 mmHg). Neither medication significantly changed electrocardiographic ST depression during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)