Marked ST Segment Depression Research Articles

Severe stenosis of the superior mesenteric artery causing an acute coronary syndrome successfully treated by percutaneous angioplasty

Pedicled gastroepiploic artery (GEA) may be used as an arterial conduit in selected patients undergoing total arterial coronary bypass grafting [1]. Myocardial ischemia may result from spasm, occlusion, and stenosis of the graft [2]. The anastomosis site at distal right coronary artery (RCA) is reported to be the most common location for stenosis of pedicled GEA bypass graft. In this work, we describe a unique case, in which the celiac artery was totally occluded and collateralized by the superior mesenteric artery which was itself severely stenosed at its ostium. Lesions manifested as an acute coronary syndrome. The patient was treated by percutaneous angioplasty with stent placement at the ostial mesenteric artery. An 84-year-old woman was referred to our intensive care unit by the emergency department for a non ST elevation myocardial infarction; EKG showed a marked ST segment depression in the lateral and inferior leads (Fig. 1) and troponin T level was elevated at 2.4 mg/l. The patient has a known history of coronary artery bypass grafting (9 years prior to admission) with a GEA to the right coronary artery, left internal mammary artery to the left anterior descending and right mammary artery to the left circumflex. She has a severe peripheral artery disease with a known occlusion of the right internal carotid artery and a total occlusion of the lower abdominal aorta. Coronary angiogram was performed through a double radial access: all the native coronary arteries were totally occluded, both internal thoracic artery grafts were patent (Fig. 2a, b). A significant ostial stenosis of the left subclavian artery was noted (Fig. 2c). We were unable to selectively opacify the celiac artery which was totally occluded. It was completely collateralized by the superior mesenteric artery which was presenting a severe ostial stenosis (Fig. 2d). A patent GEA was observable on the late frames of the mesenteric artery sequences (Fig. 2e). Given the EKG aspect of ischemia in inferior and lateral leads, we assumed that the culprit lesion was the ostial stenosis of the mesenteric artery which was ultimately responsible for the vascular supply of all the inferior territory. Through the left radial access, a balloon-expandable stent was successfully implanted with excellent immediate angiographic results (Fig. 2f, g). Given the relative frailty of the patient and the difficulty in vascular access, we decided to treat during the same procedure the high-grade stenosis of the ostial left subclavian artery which could potentially alter the flow on the left mammary artery; hence, a self-expandable stent was successfully implanted (Fig. 2h). The immediate clinical evolution was favorable; however on day 4, the patient presented a massive stroke and unfortunately expired few hours later in the coronary care unit. The present report is the first, to our knowledge, to document an ACS caused by a severe stenosis of the mesenteric artery collateralizing totally occluded celiac and gastroepiploic arteries. Although the superiority of GEA grafts over the saphenous vein grafts has never been clearly established in the setting of surgical revascularization of the RCA [3], they have been used by some surgical teams when an allarterial bypass grafting was deemed suitable. Ischemic events related to pedicled GEA grafts have been classically linked to a disease progression in the S. Rekik (&) J. Brunet F. X. Hager G. Bayet L. Meille J. M. Quatre J. Sainsous Cardiovascular Department, Clinique Rhone Durance, Avignon, France e-mail: sofienerek@yahoo.fr

Acute Coronary Syndrome Secondary to Methylphenidate Overdose

A 28‐year‐old lady presented to the emergency department after an overdose of methylphenidate. She complained of chest pain and developed an acute coronary syndrome with marked ST segment depression in the electrocardiogram and elevated troponin I level. She was closely monitored in the cardiac care unit and was treated with the standard therapy for acute coronary syndrome. Echocardiogram showed global left ventricle impairment. The follow‐up echocardiogram showed that the left ventricular function normalised and the subsequent coronary angiogram was normal. The clinical use, abuse potential, toxicity and overdose treatment of methylphenidate are discussed.

Elastin Arteriopathy and William Syndrome: Do You Feel Lucky?

To the Editor: Over the past 2 yr, we have anesthetized 10 patients with Williams syndrome and concur with the recommendations by Burch et al.1 in their recent article. In addition, we have additional suggestions based on the successful resuscitation of two infants who suffered a cardiac arrest under anesthesia. In both infants, induction of anesthesia was with incremental doses of sevoflurane (2% and 3%), a remifentanil infusion and rocuronium. Cardiac arrest occurred within 5 min of induction and before intubation. The electrocardiograms demonstrated marked ST segment depression that was followed soon after by bradycardia. Neither patient had discernible systemic output (no palpable or Doppler evidence of pulses). Resuscitation with phenylephrine, epinephrine, and small fluid boluses occurred during the institution of cardiopulmonary resuscitation. Within 5 min from the start of resuscitation, the transthoracic echocardiography (TTE) demonstrated biventricular akinesis in the first and severe biventricular hypokinesis in the second patient. We used TTE to guide our therapy, allowing us to monitor wall motion abnormalities, guide fluid administration, and carefully titrate vasopressors without worsening tachycardia or the dynamic component of subarterial outflow tract obstruction. In addition, we avoided administration of epinephrine once the rhythm returned, but pulses were still absent (pulseless electrical activity) because the TTE demonstrated severely hypertrophied, underfilled ventricles. In this population, the inappropriate administration of epinephrine as per the pediatric advanced life support protocol for pulseless electrical activity could have compromised recovery. The second patient required urgent extracorporeal membrane oxygenation cannulation after sustaining another cardiac arrest several hours after arrival in the pediatric intensive care unit within 3 min after receiving a 1 μg/kg dose of fentanyl. Both the patients underwent successful surgical repair. These patients had severe bilateral outflow track obstruction with what Stamm et al.2 have termed “macaroni pulmonary arteries” (Fig. 1). It is noteworthy that the presence of an intracardiac shunt (patent foramen ovale and small restrictive ventricular septal defect) did not decrease the risk of arrest.Figure 1.: The PA hypoplasia.Despite an induction technique designed to minimize changes in coronary perfusion, our experience demonstrates that these patients continue to have a very high-anesthetic risk of cardiac arrest. We postulate that, during induction, a decrease in coronary perfusion pressure occurred secondary to vasodilation and in combination with relative hypovolemia, and severe biventricular hypertrophy precipitated ischemia leading to cardiac arrest. In the second patient, a cardiac arrest occurred within minutes after a small dose of fentanyl, highlighting the precarious hemodynamic balance of these children. We recommend preinduction hydration, ideally with an IV, but at minimum liberal PO fluids until 2 h preinduction and the early use of TTE to help treat hemodynamic abnormalities and guide therapy. Denise C. Joffe, MD Michael Richards, BM Michael Eisses, MD Brian Emerson, MD Jeremy Geiduschek, MD Department of Pediatric Anesthesiology University of Washington Seattle, Washington [email protected]

High Altitude Arrhythmias

Objective: To investigate the cause and nature of palpitations occurring at high altitude. Methods: Implantable loop recorders were inserted subcutaneously in the left pectoral region of 9 healthy male volunteers. Subjects flew to Kathmandu (1,250 m) and then Lukla (2,800 m) before immediately commencing an identical ascent and descent profile to high altitude. The loop recorders were activated with any episode of palpitations and during exercise, rest and sleep. Arterial oxygen saturation was assessed concomitant with device activation. Results: Above 5,000 m all subjects reported palpitations during exercise. All subjects demonstrated sinus tachycardia and marked sinus arrhythmia; one subject demonstrated atrial flutter; one subject had non-conducted p waves, and a further subject had marked ST segment depression. Conclusions: Significant arrhythmias occur at high altitude. In view of the increased risk of sudden cardiac death at high altitude, and considering that the elderly account for 15% of the 100 million visitors to altitude annually, further investigation is required.

Norepinephrine-induced acute heart failure in transgenic mice overexpressing erythropoietin.

Overexpression of erythropoietin (Epo) in mice (Epo-tg6) leads to an increase in hematocrit and blood volume, and strongly reduces endurance upon exercise. It was the aim of this study to characterize the mechanisms underlying the reduced cardiac performance. Left (LV) and right (RV) ventricular function was measured with and without norepinephrine (NE) stimulation in 12 anaesthetized Epo-tg6 and in 13 wild-type (WT) control mice. There were no differences in heart function under baseline resting conditions. Stimulation with NE (10 microl bolus injections of 1-100 ng per mouse) in WT mice led to a dose-dependent increase in heart rate (HR), LV developed pressure (LVDP) and rate of rise in LV pressure (LV dP/dt(max)), while LV end-diastolic pressure (LVEDP) was unchanged. Except for HR, these parameters increased to a lesser extent in EPO-tg6 mice. Strikingly, LVEDP strongly increased in Epo-tg6 mice after NE (up to >20 mmHg). Eleven out of 13 Epo-tg6, but none of the WT mice died or required resuscitation after high-doses of NE. In these cases severe diastolic dysfunction became overt since the relative myocardial relaxation time was significantly prolonged and the duration of diastole was shortened. Moreover, the ECG showed a marked ST segment depression as well as deep negative T-waves. The NE-induced reduction in myocardial adenosin-triphosphate (ATP) content was more pronounced in Epo-tg6 mice after 10 min of continuous NE infusion (50 ng/min per mouse). NE-induced stress in Epo-tg6 mice led to acute heart failure associated with diastolic dysfunction and myocardial ischemia.

Acute infarction of the left ventricular papillary muscle: electrocardiographic pattern and recognition of its location.

ST-segment depression during acute myocardial infarction (AMI) is known to herald serious hemodynamic complications. Since the mechanism of this dependence is not clear, we reinvestigated the old concept of papillary muscle infarction (PMI) as a cause of marked ST depression. Autopsies and morpho-electrocardiographic cor-relations were performed in 53 patients with AMI involving one or both left ventricular papillary muscles, and in 10 patients with AMI, but without acute PMI. ST-segment depression > or = 1 mm in at least two leads (mean 3.6 +/- 2.2 mm) was found in 46 (86.8%) patients with, and in one without acute PMI. Thus, the sensitivity and specificity in selecting patients with acute PMI from among those with AMI were 86.8 and 90%, respectively, with an overall accuracy of diagnosis of acute PMI in the course of AMI of 87.3%. Among 26 patients with ST elevation consistent with diagnosis of AMI, ST depression, recorded in 22 patients, was insignificantly greater than in 24 of 27 patients without ST elevation: 4.1 +/- 2.9 versus 3.1 +/- 1.2 mm. Localization of ST depression in the limb leads allowed recognition of which papillary muscle suffered from acute infarction: ST depression in the inferior leads was seen only in patients with anterolateral PMI, whereas in leads I and/or a VL it was seen only in cases with posteromedial PMI. This rule was also valid in patients without concomitant ST elevation. Patients with acute PMI show marked ST-segment depression. Its location in the limb leads allows recognition of which papillary muscle has undergone necrosis. This cause of marked ST depression in patients with AMI may explain the high mortality in this particular group.

Comparison of ischemic response during exercise and dobutamine echocardiography in patients with left main coronary artery disease

This study sought to compare manifestations of myocardial ischemia evoked by exercise and dobutamine echocardiography in patients with left main coronary artery disease. During exercise testing, left ventricular cavity dilation, marked ST segment depression and blood pressure decrease indicate severe coronary artery disease. Whether these signs are comparably evoked by dobutamine echocardiography has not been described. Fifty-four patients who underwent stress echocardiography (36 exercise, 18 dobutamine) and coronary angiography showing > or = 50% left main stenosis were analyzed. Electrocardiographic and blood pressure changes, symptoms, wall motion score indexes and sensitivity for coronary artery disease were compared. In 47 patients, the left ventricular endocardium was traced to quantify volumes and ejection fraction. Stress-induced regional wall motion abnormalities developed in 91% of patients; this was not different on exercise (89%) or dobutamine echocardiography (94%). Rate-pressure product and wall motion score index, similar at rest, tended to be higher after exercise than after dobutamine stress (p = 0.07 and p = 0.05, respectively). ST segment depression > or = 1 mm was more common with exercise (p = 0.005). Ejection fraction and end-systolic and end-diastolic volume indexes were comparable at rest in both groups. With exercise, ejection fraction decreased in 87% of patients, and end-systolic and end-diastolic volume indexes increased in 80%. In contrast, with dobutamine, decreased ejection fraction and increased volume indexes were infrequent. Ejection fraction was lower ([mean +/- SD] 45 +/- 19% vs. 54 +/- 12%, p = 0.007) and end-diastolic (69 +/- 26 vs. 50 +/- 17 ml/m2, p =0.02) and end-systolic (39 +/- 20 vs. 24 +/- 13 ml/m2, p = 0.02) volume indexes were higher after exercise than after dobutamine stress. On the basis of changes in regional wall motion both dobutamine and exercise echocardiography have a comparable high sensitivity in diagnosing myocardial ischemia in left main coronary artery disease. However, conventional signs of severe myocardial ischemia, including left ventricular cavity dilation and marked ST segment depression, occur more often with exercise than with dobutamine echocardiography.

Exercise testing for assessment of the significance of ST segment depression observed during episodes of paroxysmal supraventricular tachycardia

Sixteen patients who had manifested ST segment depression during episodes of paroxysmal supraventricular tachycardia (PSVT) were studied with exercise testing in order to detect coronary artery disease and myocardial ischaemia. No ST segment depression was observed during exercise testing in 15 out of the 16 patients tested. Paroxysms of supraventricular tachycardia associated with ST segment depression occurred during exercise testing in three cases. The ST segment depression was immediately apparent, remained constant throughout the supraventricular tachycardia and was almost instantly abolished following conversion to sinus rhythm. Patients with heart rates greater than 250 beats min-1 during PSVT had marked ST segment depression associated with the tachycardia. These results suggest that coronary artery disease and myocardial ischaemia are not involved in the genesis of ST segment depression during PSVT. Tachycardia per se may be the cause of ST segment depression by altering the slope of phase 2 of the ventricular action potential. Retrograde atrial activation may also induce ST segment shifts in some of the cases.

Significance of ST segment depression during paroxysmal supraventricular tachycardia

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (± SD) of 38 ± 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias.A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 ± 12 beats/min increased to 180 ± 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 ± 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 ± 26 beats/min in five patients resulted in ≥ 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 ± 13% to −27 ± 20% (p < 0.05) indicating net myocardial lactate production.In conclusion, in patients with coronary artery disease, supraventricular tachycardia may be associated with chest pain or marked ST segment depression, or both, in the absence of acute myocardial ischemia.

Early pronounced ST segment depression with marked J point decline heralding acute lethal clinical myocardial infarction: Necropsy-electrocardiographic correlative study

Marked ST segment depression (≥ 2 mm J point decline with horizontal or downsloping ST) was correlated with necropsy findings in 105 cases. Acute myocardial infarction (AMI) was most frequently (70%) responsible for development of the abnormal ST pattern, thereby indicating the diagnosis and severe prognosis of the AMI. In 23% of patients the ST segment depression pattern was associated with chronic heart disease without AMI; all were severely ill with 92% receiving digitalis. Sudden worsening of the basic heart disease or circulatory shock were frequently found to coincide with the abnormal ST pattern; necropsy revealed extensive old MI or myocardial fibrosis in these patients. Marked ST segment depression was also found in five patients without underlying heart disease at autopsy; an acute cerebral accident or circulatory shock was considered to have produced the abnormal ST segment pattern.

965 PNEUMOPERICARDIUM: AN APPROACH TO DIAGNOSIS AND TREATMENT IN THE NEONATE

Pneumopericardium (PPC) developed in 16 of 873 (2%) neonates receiving assisted ventilation; 14 were prematures with RDS requiring assisted ventilation within 12 hours. Pneumothorax (PNX) developed coincidentally in all but one. Pericardiocentesis (PCX) was performed in 11 of whom 7 (42%) survived. Cardiovascular parameters of heart rate (HR), arterial blood pressure (ABP), central venous pressure (CVP) and ECG were measured during 10 episodes of PPC. Early evidence of cardiac tamponade (CT) was moderate tachycardia and a sharp rise in CVP. This was followed by bradycardia and an abrupt decrease in pulse and ABP. Marked ST-segment depression with AV dissociation and 2° heart block were noted at this time. Following PCX, a rebound tachycardia, widening of pulse pressure, return of ABP to baseline and a gradual fall in CVP occurred in survivors while in those who died, bradycardia and hypotension persisted. PPC as a complication of assisted ventilation should be expected in a small number of infants with RDS. If the infant develops a pneumothorax, this risk is significantly increased. The diagnosis can be made before death by cardiovascular changes described. The condition can be successfully treated and adequacy of treatment can be assessed by the same factors used for diagnosis.

Effect of beta-adrenergic blockade with alprenolol on ST-segment depression and circulatory dynamics during exercise in patients with effort angina

1. Nine subjects with severe coronary artery disease were studied during graded "sprint" and "steady-state" exercise before and after intravenous administration of the beta-receptor antagonist alprenolol. During "sprint" workload was increased every minute until maximum work capacity (Wmax) was reached. "Steady-state" exercise was performed at work rates of 0.250, 0.50, and 0.75 of each subject's sprint Wmax. Variables measured included ST-segment depression, changes in heart rate, blood pressure, respiratory gas exchange, and arterial blood composition. Cardiac output (indirect Fick) was measured during "steady-state" exercise. 2. Alprenolol did not alter Wmax during "sprint" but reduced the incidence of angina in both types of exercise. After the drug work capacity was limited by symptoms and signs suggestive of mild left ventricular failure. 3. The relationship between workload (normalized in terms of Wmax) and ST-segment depression was curvilinear. Under control conditions a given rate of work during "steady-state" exercise was assocaited with more marked ST-segment depression than during "sprint". Alprenolol displaced the work-ST-depression curve to the right in each type of exercise; now a given rate of work produced similar ST-depressing during "steady-state" and "sprint" exercise. 4. Alprenolol attentuated the exercise tachycardia during both types of exercise. Cardiac output was lower in "steady-state" exercise after the drug than under control conditions. Metabolic effects included significant reduction in body oxygen consumption after alpreprenolol at 0.25 Wmax and diminished arterial lactate at 0.75 Wmax. The beneficial effects of the drug thus appeared to involve not only cardiac but peripheral effects on beta receptors. 5. Before alprenolol cardiac output was relatively fixed at all workloads, but after the drug there was a work-related rise in output in five out of nine subjects. Comparison with data in normal subjects suggested that in anginal subjects cardiac output at low "steady-state" workloads was inappropriately high.