Transient Myocardial Ischemia Research Articles

Ostial Patch Plasty of an Aberrant Right Coronary Artery in a Symptomatic Teenager

An otherwise healthy 15-year-old girl presented with a history of transient myocardial ischemia. At the time, troponin levels were elevated to 20 microg/L. A myocardial perfusion scintigraphy evaluation revealed a minor scarring with an irreversible inferior defect at rest and at exercise. On admission, the patient was free from symptoms. Transthoracic echocardiography and computer tomography examinations revealed an aberrant origin of the right coronary artery (RCA) from the left sinus of Valsalva, just below the commissure. Repair was accomplished by incision into the RCA and patch plasty. An anomalous aortic origin of a coronary artery from the incorrect coronary sinus of Valsalva is a rare congenital cardiac defect that is associated with an increased risk of sudden death and cardiac morbidity; however, ischemia can occur even when the patient remains asymptomatic. Although this anomalous artery often shares a common orifice with the other coronary artery, it did not in the reported case. In conclusion, because of the high risk of sudden cardiac death, aggressive surgical management is indicated in symptomatic patients.

Abstract 2652: Detection of Transient Regional Myocardial Ischaemia in the Emergency Department Using a Novel Modification of Body Surface Electrocardiac Mapping is Superior to the Conventional 12 Lead ECG

Diagnosing transient regional myocardial ischaemia (TRMI) in patients presenting to the Emergency Department (ED) with acute chest pain is a challenge. The 12 lead ECG has established limitations and Troponin, though sensitive, is less reliable when used within 12 hours of symptom onset. The PRIME ECG Delta map is derived from 80 electrode electrocardiographic surface maps acquired (a) during chest pain and (b) when pain resolves. ST segment differences between scans are then displayed as colour changes on a torso map. In addition, the Ischaemic Burden (IB) - an index of the total extent of myocardial ischaemia -may be derived from the Delta Map. Objectives: In a cohort presenting with cardiac-sounding chest pain: 1.To compare the sensitivity and specificity of the PRIME Delta map and the 12 lead ECG for the diagnosis of TRMI using coronary angiography as a diagnostic gold standard. 2. To evaluate whether the IB is a valuable diagnostic tool and examine its relationship with Troponin. Methods: 80 lead ECGs were acquired for subjects with suspected TRMI when in pain and once pain free and a Delta Map derived. The IB was calculated as the sum of ST segment shift across all 80 electrodes. Subjects then underwent coronary angiography as clinically appropriate. Results: For 51 adults studied, the PRIME Delta Map was more sensitive for the detection of TRMI than the 12 lead ECG 93% vs. 81%, p 0.04. The Delta map was also more specific for TRMI 57% vs. 29%, p= 0.03.The Delta map was superior to the 12 lead particularly for detecting lateral and posterior regions of TRMI 100 % detection vs. 75%, p= 0.02. The IB correlated with peak Troponin (r= 0.52, p= 0.0001) and was significantly higher in patients with STEMI compared to NSTEMI. ROC curve evaluation of the IB showed it was an accurate measure of myocardial ischaemia with Area Under the Curve of 0.6 (95% CI 0.38 – 0.84) Conclusion: The PRIME ECG Delta map is a near patient, rapid, accurate and intuitive method for detecting TRMI and is superior to the 12 lead ECG. The IB derived from the Delta map might be a useful early surrogate for Troponin in patients with suspected TRMI. Used together, the Delta Map and IB could potentially facilitate more rapid identification and appropriate treatment in patients with coronary artery disease.

Abstract 2097: National Survey of Cardiologists’ Perceptions of Continuous ST-segment Monitoring

Continuous ST-segment (cST-seg) monitoring has been shown to help identify early and transient cardiac ischemia. American Heart Association and American Association of Critical Care Nurses recommend its use among specific patient populations. Investigators examined factors associated with cardiologists’ reported benefits, barriers, and perceptions of usefulness for cST-seg monitoring. A random sample (n=200) within a national pool of 4,985 cardiologists registered with the vendor Epocrates® was electronically surveyed. Cardiologists agreed/ strongly agreed that benefits of cST-seg monitoring included early identification of potential ischemia (83.5%), and early identification of reocclusion after PCI (74%) or fibrinolytics (72.5%). Cardiologists agreed/strongly agreed that barriers included false positive alarm for ischemia (61.5%); lack of understanding of this technology by nursing staff (56.5%); extra phone calls based on inaccurate monitoring (48%); lack of understanding of this technology by other physicians (47%); and extra cost/ treatment due to false positive alarms (43%). Cardiologists agreed/strongly agreed that cST-seg monitoring identifies patients who need further tests (69%) and is clinically useful in detecting transient myocardial ischemia (65%). The primary factor associated with higher benefits, clinical usefulness, and past use of cST-seg monitoring by cardiologists was whether or not their hospitals had a standard of practice for using cST-seg monitoring. The secondary factor was awareness of published consensus guidelines for cST-seg monitoring. Findings may indicate that when cardiologists are given the opportunity to work with a hospital that provides guidelines and experience in cST-seg monitoring, they may be more likely to appreciate its benefits and clinical utility. Clinical leaders should initiate multi-disciplinary efforts to review the level of evidence for possible incorporation of cST-seg monitoring into their hospitals’ standards of practice. Findings will help direct further research and interdisciplinary education in appropriate use of technology by critical care nurses and cardiologists.

Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease

This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0 ± 4.5 years and 12 females, aged 63.0 ± 4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3 ± 3.3 years and 13 females, aged 64.6 ± 2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1 ± 1.2 fmol/ml) were significantly ( P < 0.01) lower than those observed in normotensive patients with transient ischemia (8.2 ± 1.2 fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2 ± 1.0 fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1 ± 2.0 fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.

Sinus Node Dysfunction in Atrial Fibrillation: Cause or Effect?

Atrial fibrillation (AF) and sick sinus syndrome (SSS) are two conditions that frequently coexist. Despite a wealth of available knowledge, the link between these two entities is poorly understood. Whether AF is a harbinger of SSS or whether SSS predisposes to AF has been the subject of much debate. AF results in sinus node remodeling on a cellular and molecular basis that may promote SSS. However, not all patients with atrial fibrillation have SSS. Though “AF begets AF”, AF may also beget SSS; and SSS may also beget AF. Multiple studies have demonstrated that sinus node dysfunction may precede the onset of AF. This review will focus on alterations to sinus node structure and function, overdrive suppression, ion channel remodeling, and transient myocardial ischemia as possible mechanisms associated with AF induced SSS. In addition, we will review evidence suggesting that SSS, characterized by a combination of atrial extrasystoles, dispersion of excitability recovery and sinus node ischemia, may lead to AF. Additional factors common to both conditions such as aging and interstitial atrial fibrosis, may explain their coexistence. All this raises many therapeutic challenges associated with the interplay of AF and SSS.

Detection of acute changes in circulating troponin in the setting of transient stress test-induced myocardial ischaemia using an ultrasensitive assay: results from TIMI 35

To determine whether an ultrasensitive assay can permit quantification of changes in circulating cardiac troponin (Tn) in the setting of stress test-induced myocardial ischaemia. Blood samples were obtained before, immediately after, and 2 and 4 h after stress testing with nuclear perfusion imaging in 120 patients. Troponin was measured using commercial assays as well as with a novel, ultrasensitive cardiac TnI assay with a limit of detection of 0.2 pg/mL. Using the ultrasensitive assay, TnI was detectable in all patients before stress testing (median 4.4 pg/mL, interquartile range 3.1-8.6 pg/mL). By 4 h, troponin levels were unchanged in patients without ischaemia, whereas circulating levels had increased by a median of 1.4 pg/mL (24% increase) in patients with mild ischaemia (P = 0.002) and by 2.1 pg/mL (40% increase) in patients with moderate-to-severe ischaemia (P = 0.0006). In contrast, changes in troponin levels across patients in different ischaemic categories were indistinguishable using commercial troponin assays. When added to clinical factors, a >1.3 pg/mL increase in TnI using the ultrasensitive assay was an independent predictor of ischaemia (odds ratio 3.54, P = 0.007). Transient stress test-induced myocardial ischaemia is associated with a quantifiable increase in circulating troponin that is detectable with a novel, ultrasensitive TnI assay.

Proteomic analysis of left ventricular tissues following intermittent myocardial ischemia during coronary collateralization in rabbits

Background Repeated transient myocardial ischemia may offer favorable effects to coronary perfusion via collateral circulation, although the underlying molecular mechanisms still remain unclear. This study was designed to evaluate the proteomic changes during this process. Methods Rabbits were randomly divided into sham-operated and ischemic groups (5 each) and were subjected to intermittent myocardial ischemia by inflation or deflation of pneumatic occluders for 4 weeks to establish a controlled myocardial ischemic model. Isolated hearts were subjected to histological observation, microspheric detection, capillary counting and proteomic analysis. Results Elevation of ST segment or back to normal in Lead-II electrocardiogram could be induced by occluders without overt histological and cardiac troponin I alterations. Regional coronary collateral blood flow exhibited a remarkable increase following intermittent inflation of occluders in the ischemic group ( P < 0.01). Simultaneously, capillary numbers per unit area were significantly different between groups ( P < 0.01). Twenty-three differentially expressed protein spots were separated by two-dimensional gel electrophoresis and 13 out of them were identified by MALDI-TOF-MS. Conclusion The present study indicates that the differentially expressed proteins involved in proliferation, growth and energy metabolism following intermittent myocardial ischemia without ischemia-reperfusion injury are likely associated with the development of collateralization beneficial to coronary circulation.

Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

IntroductionArginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.MethodsCardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).ResultsAVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.ConclusionLow dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.

Acute Metformin Therapy Confers Cardioprotection Against Myocardial Infarction Via AMPK-eNOS–Mediated Signaling

Clinical studies have reported that metformin reduces cardiovascular end points of type 2 diabetic subjects by actions that cannot solely be attributed to glucose-lowering effects. The therapeutic effects of metformin have been reported to be mediated by its activation of AMP-activated protein kinase (AMPK), a metabolite sensing protein kinase whose activation following myocardial ischemia has been suggested to be an endogenous protective signaling mechanism. We investigated the potential cardioprotective effects of a single, low-dose metformin treatment (i.e., 286-fold less than the maximum antihyperglycemic dose) in a murine model of myocardial ischemia-reperfusion (I/R) injury. Nondiabetic and diabetic (db/db) mice were subjected to transient myocardial ischemia for a period of 30 min followed by reperfusion. Metformin (125 microg/kg) or vehicle (saline) was administered either before ischemia or at the time of reperfusion. Administration of metformin before ischemia or at reperfusion decreased myocardial injury in both nondiabetic and diabetic mice. Importantly, metformin did not alter blood glucose levels. During early reperfusion, treatment with metformin augmented I/R-induced AMPK activation and significantly increased endothelial nitric oxide (eNOS) phosphorylation at residue serine 1177. These findings provide important information that myocardial AMPK activation by metformin following I/R sets into motion events, including eNOS activation, which ultimately lead to cardioprotection.

Estimated body surface potential maps in emergency department patients with unrecognized transient myocardial ischemia

Background We report on 5 patients who presented to the emergency department (ED) with chest pain, had negative serum troponin levels, and were discharged with a presumed noncardiac diagnosis. Thereafter, retrospective analysis of Holter monitoring data recorded for a clinical trial revealed ST events indicative of transient myocardial ischemia that was unrecognized clinically. Study Aim The purpose of this analysis was to determine whether initial body surface potential maps estimated from optimal ischemia electrode sites estimated body surface potential map (EBSPM) showed signs of ischemia in the missed ischemia group that could have prevented misdiagnosis. Methods This is a secondary analysis of data from a prospective clinical trial in which patients were attached to 2 Holter monitor devices for simultaneous recordings. One Holter device recorded a standard Mason-Likar 12-lead electrocardiogram (ECG) and the other recorded a 10-electrode lead set considered optimal for ischemia detection. A body surface potential map was then estimated from the optimal lead set. Results At 1 year, 2 of the 5 patients with missed ischemia died and a third had an acute myocardial infarction (MI) (40% mortality, 60% death/nonfatal MI). In comparison, 1-year mortality was 5.7% in 159 similar patients treated for unstable angina at the same institution over the same period ( P = .037). The initial standard ECG showed no abnormalities in 3 patients and showed left ventricular hypertrophy in 1. The fifth patient with a history of recent MI had slight ST elevation in leads III and aVF and Q waves that were considered indicative of recent (not acute) MI. EBSPM data recorded at the time of ED presentation matched the standard ECG (normal in 3, left ventricular hypertrophy or inconclusive in 2). During transient ischemia, all 5 EBSPMs showed areas of ischemia overlapping with standard electrode sites. Conclusion Patients evaluated in the ED for chest pain are at high risk for death or nonfatal MI if they have ischemic events with continuous ST-segment monitoring that are unrecognized clinically. In this small cohort with unrecognized ischemia, the initial body surface potential maps estimated from optimal ischemia electrode sites did not improve on 12-lead ST-segment monitoring to identify this high-risk group.

Dynamic tracking of ischemia in the surface electrocardiogram

Background Accurate detection of the earliest signs of ischemia on the surface electrocardiogram (ECG) is essential for timely diagnosis and management of potentially life-threatening ischemic events. Yet, accuracy of ischemia analysis in ECG monitors remains suboptimal because of a number of confounding factors, including changes in body position and other artifacts. Hence, the goals of this study were (1) to examine the duration and time course of ischemic events and (2) to compare ECG changes caused by “true” ischemic events with those caused by changes in body position. Continuous, 12-lead Holter ECGs obtained from patients who presented to the emergency department with chest pain and enrolled in the Ischemia Monitoring and Mapping in the Emergency Department in Appropriate Triage and Evaluation of Acute Ischemic Myocardium study were analyzed. Holter recordings were initiated within the first 40 minutes after patients' arrival to the emergency department. Here we present preliminary results. Methods Twelve patients (age, 59 ± 16 years; 5 women, 2 with a final diagnosis of non–ST-segment elevation myocardial infarction, 4 with unstable angina, and 6 with other cardiovascular diseases), in whom ischemic ST deviations were identified on Holter data, underwent 4 consecutive, 2-minute recordings in the following body positions: (1) supine, (2) on the left side, (3) on the right side, and (4) sitting (or standing) upright. After baseline correction, beat-to-beat changes in QRS and ST-T segments were examined in all 8 channels and the root-mean-square curve by using an adaptive algorithm that computes the slope, amplitude, duration, area, and the Karhunen-Loève–derived representation of the corresponding segment. To prevent possible biases toward patients with more frequent ischemic events, a single index event was chosen for analysis in each patient. There were 3 ST-elevation events and 9 ST-depression events; these events reached the maximum ST deviation 11 ± 8 hours (mean ± SD) after the beginning of the recording. Results and Conclusions In most patients with transient myocardial ischemia, the microvolt-level, subthreshold deviation of the ST segment developed gradually, over 15 to 20 minutes, until it reached the maximum, superthreshold level. Despite the different ischemia localizations, the root-mean-square curve allowed accurate detection of significant changes in the ST segment in the studied group (Friedman analysis of variance for repeated measurements over a 1-hour interval). Changes in body position could be identified by tracking dynamics of the QRS pattern/axis. Adaptive algorithms for tracking of the ST dynamics with simultaneous tracking of the patterns of QRS complexes to discriminate the true and “false”-positive events are presented and discussed.

Do Men and Women Differ on Measures of Mental Stress-Induced Ischemia?

To consider the effects of gender on ischemia in a larger sample, with broadly defined coronary artery disease (CAD). Mental stress has been shown to cause transient myocardial ischemia in a significant percentage of people with CAD. However, little is known about the effects of mental stress on ischemic processes in women. Most studies to date either had few women or required a positive exercise stress test. Participants (61 women, 93 men; average age = 63 years) had documented CAD (positive stress test, abnormal catheterization even with minimal disease, or previous myocardial infarction). They underwent mental stress testing and radionuclide perfusion imaging (stress/ rest). Cardiac function data were collected and stress was compared with baseline. The data were then submitted to a series of analyses of variance. A total of 50 (32%) participants exhibited reversible ischemia post psychological stress. This reflects a relative rate of 33% (n = 31 of 93) for men and 31% (n = 19 of 61) for women. No difference between men and women were observed on any measure of hemodynamic functioning (blood pressure, heart rate, or cardiac perfusion). Results of this study showed no significant differences between men and women on measures of hemodynamic functioning or cardiac perfusion.

Serum deoxyribonuclease I activity can be used as a novel marker of transient myocardial ischaemia: results in vasospastic angina pectoris induced by provocation test

Serum deoxyribonuclease I (DNase I) activity has recently been highlighted as a potential diagnostic marker for detection of acute myocardial infarction. To evaluate whether serum DNase I activity is useful for detection of myocardial ischaemia, we investigated alteration of its levels after onset of vasospastic angina pectoris (VSAP), resulting in transient myocardial ischaemia, induced by the intracoronary ergonovine provocation test. Twenty-nine consecutive patients with suspected VSAP were subjected to the test. Patients were categorized as VSAP-positive (n = 13) or -negative (n = 16) based on development of angina. Serum samples were examined for DNase I activity before, immediately after, and 3, 6, and 24 h after the provocation tests. The serum DNase I activity increased significantly from the baseline 3 h after the provocation test in 11 patients of the VSAP-positive group whose levels of troponin T were within the normal range. Median of the percentage differences from the baseline in serum DNase I activity 3 h after the test was 32.1% (25th and 75th percentile: 28.6 and 42.0%, respectively; P = 0.000012). In the VSAP-negative group, levels of DNase I activity remained unchanged at any point of time after the provocation test. Transient myocardial ischaemia resulting from VSAP induces a significant elevation of serum DNase I activity. Therefore, serum DNase I activity may be applicable as a useful marker for detecting transient myocardial ischaemia.

Abstract 3108: Single Molecule Troponin Detection to Assess for Transient Myocardial Ischemia

Background : It has been proposed that small amounts of cardiac troponin (Tn) may be released from myocytes in the setting of reversible myocardial injury. We hypothesized that a more sensitive Tn assay could permit the quantification of transient myocardial ischemia. Methods : Blood samples were obtained before and 4 hrs after stress testing with perfusion imaging in 99 pts w/o recent angina. Tn was measured using the current generation TnT assay (Roche, limit of detection, LOD, 0.01 ng/ml) and the new Singulex TnI assay, which, using single molecule counting technology, has a LOD 50 fold lower (0.2 pg/ml). Pts were categorized by severity of ischemia on perfusion imaging; median changes in Tn levels were compared across ischemic groups. Results : Using the Singulex assay, TnI was detectable in all pts before stress testing (median 4.4 pg/ml). The median duration of angina during testing was 0, 0, and 3 mins in pts with none, mild, and mod/sev ischemia. By 4 hrs, TnI levels were unchanged in pts w/o ischemia, whereas circulating levels had significantly increased by 1.37 pg/ml (24%) in pts with mild ischemia (P=.002) and by 2.08 pg/ml (40%) in pts with mod/sev ischemia (P=.0006) (Fig ). In a multivariable model that included mins of exercise, angina, and ST changes, change in TnI was a significant predictor of ischemia (OR 3.36, P=.03). In contrast, using the existing TnT assay there were no detectable differences in Tn levels (median difference 0.00 ng/ml in all groups). Conclusion : A 50-fold more sensitive troponin assay can quantify rises in circulating troponin in patients experiencing brief, provoked myocardial ischemia. The clinical applications of such assays warrant further study.

Exercise‐Induced ST‐Segment Elevation in Patients with a Recent Acute Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention

To get insight in the mechanism of exercise-induced ST-segment elevation (STE) in patients with Q/QS waves at the electrocardiogram (ECG). We performed exercise stress test in 13 patients with anterior acute myocardial infarction treated by successful primary percutaneous coronary intervention (PCI). Compared to rest, an additional STE > or = 1 mm in one or more precordial ECG leads during exercise occurred in nine patients (69%), in the absence of symptoms. In acute myocardial infarction (MI) patients, treated by primary PCI and showing optimal coronary blood flow restoration at angiography, STE can still be induced by exercise in Q/QS wave ECG leads. This finding lends further support to the theory that exercise-induced STE in this clinical context is unlikely to represent by itself transient myocardial ischemia or viability.

Sympathetic neural responses to coronary occlusion during balloon angioplasty

The sympathetic nervous system is a key modulator of prognosis and outcome in cardiac ischaemia and infarction. The effects of acute cardiac ischaemia on sympathetic neural traffic in humans are unknown. We tested the hypothesis that angioplasty, and associated transient myocardial ischaemia, elicits changes in neural circulatory control, including direct intraneural measures of sympathetic traffic. We measured muscle sympathetic nerve activity (MSNA), blood pressure and heart rate in 12 patients (11 men, one woman) undergoing clinically indicated elective coronary angioplasty of the left anterior descending (n = 7) or circumflex (n = 5) coronary artery. Baseline data were obtained for 2 min before occlusion. Each balloon inflation was designed to last up to 120 s. Coronary occlusion had no significant effect on blood pressure or heart rate. In contrast, occlusion resulted in a significant increase in MSNA, in 10 of the 12 patients, and in all seven of those patients undergoing angioplasty of the left anterior descending artery. The group mean increase in MSNA during occlusion was 36 +/- 11% (P = 0.008 versus preocclusion). MSNA increased within 60 s of occlusion (129 +/- 12% of baseline; n = 12; P = 0.04), and increased further during the next 60 s to 141 +/- 12% of baseline levels (n = 10; P < 0.001). Increases in MSNA were similar in patients with and without significant chest pain (39 +/- 9% versus 34 +/- 13%, respectively; P = 0.84). Acute coronary occlusion during angioplasty increases central sympathetic outflow, but there is no systematic change in heart rate. The increase in sympathetic nerve traffic cannot be explained by blood pressure changes or occlusion-related chest pain.

‘Silent’ Prinzmetal’s ST Elevation Related to Atenolol Overdose

Prinzmetal’s angina is a condition characterized by chest pain, transient ST elevation, and negative biochemical markers of myocardial cell necrosis. We describe a case of chemically-induced “silent” ST segment elevation related to Atenolol overdose in a patient without coronary artery stenosis. We conclude that the cause for the transient myocardial ischemia is coronary vasospasm, precipitated by beta-blocker overdose.

Treating Ischemic Left Ventricular Dysfunction With Hypertonic Saline Administered After Coronary Occlusion in Pigs

The effects of hypertonic saline on ventricular function are controversial, whether it is increasing contractility or preload. There are no data, however, on the influence of hypertonic saline in a stunned myocardium. This study was prospective and randomized in order to analyze the effects of hypertonic saline solution (7.5%) on myocardial function and systemic hemodynamics in a porcine model of ischemia and reperfusion. A university teaching hospital, animal research laboratory. Twelve adult domestic swine. Myocardial stunning was produced by the complete occlusion of the proximal left anterior descending artery for 15 minutes followed by reperfusion. Five minutes after reperfusion, the animals were assigned to receive 4 mL/kg of hypertonic saline (n = 7) or normal saline (n = 5) over 10 minutes. Pressure-tipped catheters were placed in the left ventricular cavity and aorta. The dimensions of the left ventricle were measured with ultrasonic microcrystals. Cardiac output was measured with transit time ultrasound. Data were recorded continuously and compared before the occlusion, 5 minutes after reperfusion, and at the end of the infusion. Compared with baseline, ventricular function was significantly depressed after left anterior descending artery occlusion. Left ventricular dP/dT and its end-systolic pressure-volume slope decreased (38% and 52%, respectively; p < 0.05), with a concomitant increase in systemic vascular resistance. The administration of hypertonic saline significantly improved left ventricular function (Emax 1,422 +/- 198 mmHg/mL, and dP/dT 3.2 +/- 0.4 mmHg/s v normal saline group values of 1,156 +/- 172 and 2.5 +/- 0.5, respectively; p < 0.05), cardiac output (2.5 +/- 0.5 v 1.84 +/- 0.4 L/min, p < 0.05), and lowered systemic vascular resistance (from 28.8 +/- 2.3 to 23.5 +/- 1.4, p < 0.05), with no significant changes with normal saline administration. After transient myocardial ischemia, hypertonic saline administered over a short period of time acts as an inodilator by increasing contractility while simultaneously lowering systemic vascular resistance.

Élévation de la sécrétion du Nt-proBNP dans les 24 heures suivant une angioplastie coronaire : à propos de 90 cas

Nt-proBNP have emerged as useful biomarker for the diagnosis and prognostic of heart failure but also recently in acute coronary syndrome. Myocardial ischemia is probably an important stimulus for Nt-proBNP release. Transient myocardial ischemia is inducing by balloon inflation during percutaneous coronary intervention (PCI). The authors propose to determine the Nt-proBNP secretion after uncomplicated coronary intervention in patients with preserved cardiac function. Ninety patients were enrolled in this study. Plasma Nt-proBNP was increased significantly from 135.5 to 157.8 pg/ml and 202.5 pg/ml at 8 and 24 hours following PCI, respectively. History of myocardial infarction and complex lesions were the most powerful predictors of higher Nt-proBNP peak concentration. Prognostic value must be evaluated in larger studies.

Ischemia-modified albumin is a highly sensitive serum marker of transient myocardial ischemia induced by coronary vasospasm

Ischemia-modified albumin, a new marker of myocardial ischemia, is known to elevate during ischemia induced by percutaneous coronary intervention. It is, however, not known whether ischemia-modified albumin also elevates during transient coronary vasospasm. We evaluated ischemia-modified albumin in patients undergoing intracoronary ergonovine spasm provocation test (n=26). For additional comparison, ischemia-modified albumin was also evaluated in elective percutaneous coronary intervention patients (n=18) and in patients with normal coronary angiography (n=10). Blood samples were taken from the arterial sheath before the procedure, just after procedural completion, or balloon inflation. Median ischemia-modified albumin level elevated significantly in patients with positive provocation test compared with baseline [n=16, 106.0 (interquartile range 96.5, 115.5) versus 128.5 (114.8, 171.8) U/ml, P<0.001], whereas it did not change in patients with negative provocation test [n=10, 109.5 (103.3, 115.0) versus 113.5 (104.0, 118.3) U/ml, P=0.108]. Ischemia-modified albumin was also higher after percutaneous coronary intervention [113.5 (101.0, 131.5) versus 151.0 (129.3, 231.0) U/ml, P<0.0001] and did not change in patients with normal coronary angiography [108.5 (99.3, 114.0) versus 110.0 (108.0, 114.0) U/ml, P=0.085]. Ischemia-modified albumin elevation higher than 9 U/ml after provocation test could detect the presence of coronary vasospasm, with an area under the receiver operating characteristic curve of 0.975 (95% confidence interval 0.921-1.000), with a sensitivity of 94% and a specificity of 99%. Serum albumin levels were within reference range for all patients and there was no significant relationship between albumin and baseline ischemia-modified albumin or postischemic ischemia-modified albumin. Thus, ischemia-modified albumin may have a role as a biochemical marker for transient myocardial ischemia induced by coronary vasospasm.