Differential distribution of 5HT1D- and 5HT1B-immunoreactivity within the human trigemino-cerebrovascular system: implications for the discovery of new antimigraine drugs

Sumatriptan, a 5HT_1B/1D-receptor agonist, is clinically effective as an antimigraine agent. Its therapeutic action may result partly from vasoconstriction of excessively dilated cranial blood vessels (a 5HT_1B-receptor mediated response). The antimigraine activity of sumatriptan may also result from inhibition of the release of vasoactive neuropeptides from trigeminal sensory fibres within the meninges. The identity of the 5HT_1B/1D-receptor subtype mediating this effect is unknown. Using 5HT_1D- and 5HT_1B-receptor-specific antibodies we have demonstrated a differential distribution of these receptor subtypes within the human trigemino-cerebrovascular system. Only 5HT_1B-receptor protein was detected on dural arteries. In contrast, only 5HT_1D-receptor protein was detected on trigeminal sensory neurones including peripheral and central projections to dural blood vessels and to the medulla. Within the medulla 5HT_1D-receptor protein was confined to discrete areas associated with the trigeminal sensory system. These findings have important implications for the design of new antimigraine drugs.     

Serotonin type 1D receptors (5HTR) are differentially distributed in nerve fibres innervating craniofacial tissues

We tested the hypothesis that the 5HT_1DR, the primary antinociceptive target of triptans, is differentially distributed in tissues responsible for migraine pain. The density of 5HT_1DR was quantified in tissues obtained from adult female rats with Western blot analysis. Receptor location was assessed with immunohistochemistry. The density of 5HT_1DR was significantly greater in tissues known to produce migraine-like pain (i.e. circle of Willis and dura) than in structures in which triptans have no antinociceptive efficacy (i.e. temporalis muscle). 5HT_1DR-like immunoreactivity was restricted to neuronal fibres, where it colocalized with calcitonin gene-related peptide and tyrosine hydroxylase immunoreactive fibres. These results are consistent with our hypothesis that the limited therapeutic profile of triptans could reflect its differential peripheral distribution and that the antinociceptive efficacy reflects inhibition of neuropeptide release from sensory afferents. An additional site of action at sympathetic efferents is also suggested.     

Differential effects of the 5HT1B/1D receptor agonist naratriptan on trigeminal versus spinal nociceptive responses

In vivo electrophysiological assays in anesthetized rats have been used to compare the effects of the 5HT_1B/1D receptor agonist, naratriptan, on central trigeminal nociceptive processing from dural and cutaneous inputs with its effects on nociceptive processing in the spinal cord. Naratriptan inhibited responses of single trigeminal neurons, to noxious electrical and mechanical stimulation of the dura and face, dose dependently by a maximum of 67±3% and 70±18%, respectively, at 3 mg kg⁻¹ i.v. In contrast, naratriptan did not affect spinal dorsal horn neuronal responses to noxious mechanical stimulation of the hind-paw. These findings suggest that 5HT_1B/1D receptors have differential effects on nociceptive processing in the trigeminal versus spinal dorsal horns and provide a potential explanation for the lack of general analgesic effects of brain penetrant 5HT_1B/1D agonist antimigraine drugs.     

Role of "Ischemia modified albumin", a new biochemical marker of myocardial ischaemia, in the early diagnosis of acute coronary syndromes

Background: Diagnosis of cardiac ischaemia in patients attending emergency departments (ED) with symptoms of acute coronary syndromes is often difficult. Cardiac troponin (cTn) is sensitive and specific for the detection of myocardial damage but may not rise during reversible myocardial ischaemia. Ischemia Modified Albumin (IMA) has recently been shown to be a sensitive and early biochemical marker of ischaemia. Methods and Results: This study evaluated IMA in conjunction with ECG and cTn in 208 patients presenting to the ED within three hours of acute chest pain. At presentation, a 12-lead ECG was recorded and blood taken for IMA and cardiac troponin T (cTnT). Patients underwent standardised triage, diagnostic procedures, and treatment. Results of IMA, ECG, and cTnT, alone and in combination, were correlated with final diagnoses of non-ischaemic chest pain, unstable angina, ST segment elevation, and non-ST segment elevation myocardial infarction. In the whole patient group, sensitivity of IMA at presentation for an ischaemic origin of chest pain was 82%, compared with 45% of ECG and 20% of cTnT. IMA used together with cTnT or ECG, had a sensitivity of 90% and 92%, respectively. All three tests combined identified 95% of patients whose chest pain was attributable to ischaemic heart disease. In patients with unstable angina, sensitivity of IMA used alone was equivalent to that of IMA and ECG combined. Conclusions: IMA is highly sensitive for the diagnosis of myocardial ischaemia in patients presenting with symptoms of acute chest pain.     

Peripheral vascular effects and pharmacokinetics of the antimigraine compound, zolmitriptan, in combination with oral ergotamine in healthy volunteers

Members of the new class of antimigraine compounds, 5HT_1B/1D agonists, as well as ergotamine, may cause vasoconstriction through stimulation of 5HT receptors on peripheral vessels. The cardiovascular effects of 20 mg oral zolmitriptan (Zomig, formerly 311C90), 2 mg oral ergotamine and the combination were assessed in a randomized double-blind, placebo-corirolled crossover study in 12 healthy subjects. Pharmacodynamic measures included oscillometric blood pressure, systolic blood pressure at the toe and arm using a strain gauge technique, stroke volume and cardiac output using bioimpedance cardiography, high-resolution ultrasound to measure brachial arterial diameter and a novel Doppler method to measure blood flow velocity. Both drugs produced small degrees of peripheral vasoconstriction, including increases in diastolic blood pressure and blood flow velocity and decreases in arterial diameter and toe-arm systolic pressure gradient. These effects were generally additive with the combination but of no clinical importance. There were no significant changes in cardiac output, stroke volume heart rate or ECG. Zolmitriptan, at eight times the likely therapeutic dose, was generally well tolerated both alone and in combination with ergotamine. Ergotamine had no clinically important effects on zolmitriptan pharmacokinetics.     

311C90 (Zolmitriptan*), a novel centrally and peripheral acting oral 5-hydroxytryptamine-1D agonist: a comparison of its absorption during a migraine attack and in a migraine-free period

The oral absorption of a 10-m. oral dose of the novel 5-hydroxytryptamine (5HT_1D) agonist, 311C90, was compared during a moderate or severe migraine headache and in a migraine-free period in an open, two-period study. The safety and efficacy of 311C90 in acute migraine were also assessed. Twenty patients attended the clinics during a moderate or severe migraine attack and 18 patients returned for a second dose in a migraine-free period 311C90 was less rapidly absorbed during a migraine attack compared to the migraine-free period, cons stent with gastric stasis during a migraine attack. The median area under the curve (AUC) was 15.7 ng/mlh lower during a migraine (median AUC: 18.4ng/ml.h, range: 0–60.8 ng/ml.h) compared to the migraine-free period (median AUC: 33.4 ng/ml.h, range 9.4–79.5 ng/ml.h) (95% confidence interval: 6.9,25.3) and the time to reach maximum plasma concentration was delayed ( n = 18). Eleven out of 20 patients experienced a significant improvement in migraine headache intensity at 2 h post-dose. Plasma 311C90 concentrations were generally higher in those patients who responded to treatment with 311C90 in the plasma, but there was one patient with no quantifiable 311C90 in the plasma whose headache improved. Minor adverse experiences were reported in 11 out of 20 patients during a migraine attack and in 11 out of 18 patients outside an attack. They occurred shortly following drug administration and were of short duration, but their occurrence did not appear to be related to plasma 311C90 concentration. There were no clinically significant changes in blood pressure or 12-lead ECG during the assessment period.     

Autoradiographic distribution of [3H]sumatriptan-binding sites in post-mortem human brain

The anatomical distribution of [³H]sumatriptan-binding sites was analysed in brain tissue sections from 11 subjects. Relevant concentrations of [³H]sumatriptan-binding sites were seen in areas such as visual cortex>locus niger>globus pallidus>layers IV-V of the frontal cortex>subiculum>entorhinal cortex>nucleus tractus solitarius>nucleus trigeminalis caudalis. This distribution of [³H]sumatriptan-binding sites in the human brain shows some differences when compared with that of 5HT_1D receptors, confirming that, besides 5HT_1D,sumatriptan also binds to 5HT_1F receptor subtype. Some species differences are evident between the distribution of [³H]sumatriptan-binding sites in the human brain and that reported for guinea-pig and rat brains, emphasizing that caution is needed in extrapolating experimental data from animals to humans. Furthermore, these data help to explain some of the therapeutic actions of sumatriptan. The remarkable levels of binding found in areas such as nucleus tractus solitarius and nucleus trigeminalis caudalis suggest that in migraine attacks sumatriptan could exert its specific anti-emetic effects and, partly at least, induce analgesia by directly acting over these brain nuclei.     

Naratriptan: biological profile in animal models relevant to migraine

The biological profile of naratriptan (N-methyl-3-(1-methyl-4-piperidinyl)-1H-indole-5-ethane-sulphona-mide), a novel 5HT_1B/1D receptor agonist, was investigated in a variety of experimental models of relevance to migraine. Naratriptan has high affinity for human recombinant 5HT_1B and 5HT_1D receptors (pKi = 8.70.03 and 8.30.1, respectively) and causes contractions of dog isolated basilar and middle cerebral artery (EC₅₀ values of 0.11 and 0.07 M, respectively). Naratriptan causes small contractions of human isolated coronary arteries (EC₅₀ value of 0.17 M; maximum contraction equivalent to 33% of 5HT maximum). In anaesthetized dogs, naratriptan causes selective vasoconstriction of the carotid arterial bed (CD₅₀ dose = 193 g kg⁻¹) and, in anaesthetized rats, naratriptan selectively inhibits neurogenic plasma protein extravasation in the dura (ID₅₀ = 4.1 g kg⁻¹). In a variety of antinociceptive tests, naratriptan has no effect even at high doses. In conscious rats and dogs, naratriptan has high oral bioavailability (71% and 95%, respectively). The data show that naratriptan is a selective agonist at 5HT_1B/1D receptors, with a pharmacological profile very similar to that of sumatriptan, albeit 2-3 fold more potent. These observations, coupled with high oral bioavailability in animals, suggest that naratriptan has the profile of an orally effective anti-migraine drug.     

Acute myopericarditis with focal ECG findings mimicking acute myocardial infarction

Background: Although history, physical examination, laboratory data points, and electrocardiogram (ECG) are helpful, distinguishing among pericarditis, myopericarditis, and myocardial infarction can be difficult. Objectives: This case, which presents as pericarditis with concomitant myocarditis (myopericarditis), illustrates the four evolving ECG stages of pericarditis and highlights some of the potential difficulties in differentiating between myopericarditis and acute myocardial infarction. Case Report: We present the case of a previously healthy 15-year-old boy who presented to the Emergency Department (ED) from his family physician's office for chest pain and presumed pericarditis. The patient's initial ECG showed infero-lateral ST-segment elevation, and his troponin T was elevated at 1.54 ng/mL (ref. < 0.03). Several hours after presentation to the ED, the patient experienced “10/10” chest pain, and a repeat ECG showed ST elevation increased from the prior ECG. After an emergent echocardiogram revealed no regional wall abnormalities, he was transferred to a pediatric cardiac intensive care unit, where a heart catheterization revealed no coronary irregularities. He was discharged 4 days later with the diagnosis of myopericarditis. Conclusion: This case report illustrates some of the difficulties in differentiating among myopericarditis and myocardial infarction in a 15-year-old patient presenting with chest pain.     

Intensity dependence of the cortical auditory evoked potentials as a surrogate marker of central nervous system serotonin transmission in man: demonstration of a central effect for the 5HT1B/1D agonist zolmitriptan (311C90, Zomig ®).

As shown in animal studies, 5HT_1B/1D agonists can inhibit activity in the trigeminal nucleus caudalis, which may be advantageous for their antimigraine effect. To demonstrate a possible central nervous system (CNS) action of these compounds in man we studied their effect on the intensity dependence of the cortical auditory evoked potentials (IDAPs), thought to be inversely related to central serotonergic transmission. An amplitude/stimulus intensity function (ASF) slope was computed in healthy volunteers and migraine patients between attacks before and 2 h after oral 311C90 (zolmitriptan "Zomig") 10 mg ( n =14), 311C90 5 mg ( n =7), sumatriptan 100 mg ( n =14), dexfenfluramine 15 mg ( n =4), lorazepam 1.25 mg ( n =4) and placebo ( n =14). 311C90 10 mg and, to a lesser degree, 5 mg significantly increased the mean ASF slope ( p =0.007 and 0.05 vs placebo). There was a significant positive correlation between plasma levels of 311C90 and ASF slope changes. Sumatriptan and lorazepam had little effect, but dexfenfluramine produced a significant ASF slope decrease. 311C90 is able to modify a CNS activity that is modulated by serotonin, i.e. the IDAP. This effect is probably the consequence of its super or lipophilicity compared to sumatriptan and of activation of prejunctional 5HT_1B/1D autoreceptors, which lowers central serotonin release and thus the preactivation level of sensory cortices.     

Frequency of Acute Coronary Syndrome in Patients with Normal Electrocardiogram Performed during Presence or Absence of Chest Pain

Objectives: The authors hypothesized that patients with active chest pain at the time of a normal electrocardiogram (ECG) have a lower frequency of acute coronary syndrome (ACS) than patients being evaluated for chest pain but with no active chest pain at the time of a normal ECG. The study objective was to describe the association between chest pain in patients with a normal ECG and the diagnosis of ACS. Methods: This was a prospective observational study of emergency department (ED) patients with a chief complaint of chest pain and an initial normal ECG admitted to the hospital for chest pain evaluation over a 1-year period. Two groups were identified: patients with chest pain during the ECG and patients without chest pain during the ECG. Normal ECG criteria were as follow: 1) normal sinus rhythm with heart rate of 55–105 beats/min, 2) normal QRS interval and ST segment, and 3) normal T-wave morphology or T-wave flattening. “Normal” excludes pathologic Q waves, left ventricular hypertrophy, nonspecific ST-T wave abnormalities, any ST depression, and discrepancies in the axis between the T wave and the QRS. Patients’ initial ED ECGs were interpreted as normal or abnormal by two emergency physicians (EPs); differences in interpretation were resolved by a cardiologist. ACS was defined as follows: 1) elevation and characteristic evolution of troponin I level, 2) coronary angiography demonstrating >70% stenosis in a major coronary artery, or 3) positive noninvasive cardiac stress test. Chi-square analysis was performed and odds ratios (ORs) are presented. Results: A total of 1,741 patients were admitted with cardiopulmonary symptoms; 387 met study criteria. The study group comprised 199 males (51%) and 188 females (49%), mean age was 56 years (range, 25–90 years), and 106 (27%) had known coronary artery disease (CAD). A total of 261 (67%) patients experienced chest pain during ECG; 126 (33%) patients experienced no chest pain during ECG. There was no difference between the two groups in age, sex, cardiac risk factors, or known CAD. The frequency of ACS for the total study group was 17% (67/387). There was no difference in prevalence of ACS based on the presence or absence of chest pain (16% or 42/261 vs. 20% or 25/126; OR = 0.77, 95% confidence interval = 0.45 to 1.33, p = 0.4). Conclusions: Contrary to our hypothesis concerning patients who presented to the ED with a chief complaint of chest pain, our study demonstrated no difference in the frequency of acute coronary syndrome between patients with chest pain at the time of acquisition of a normal electrocardiogram and those without chest pain during acquisition of a normal electrocardiogram.     

Myocardial injury in a patient with severe coronavirus disease: A case report

IntroductionCoronavirus disease (COVID-19) can lead to severe disease or death and is characterized by a wide range of mild to severe symptoms. In addition to the lungs, studies have reported the involvement of the stomach, intestine, and angiotensin-converting enzyme 2 receptors in the heart.Case reportWe present a case of a patient with COVID-19 who died soon after developing multi-organ failure and myocardial injury due to COVID-19-associated pneumonia. A 71-year-old man who contracted COVID-19 was admitted to the hospital after presenting with fever for 7 days and developed dyspnea. Following treatment, his respiratory status worsened. Thus, he was transferred to our hospital for intensive care on day 11. Physical examination revealed fever, dyspnea, respiratory distress, and no chest pain. Invasive positive pressure ventilation was initiated for acute respiratory distress syndrome on day 14. On day 15, we observed renal, liver, and coagulation dysfunction, indicating multi-organ failure. Chest radiography did not show clear signs of an increased cardiothoracic ratio or pulmonary congestion. An electrocardiogram (ECG) showed signs of myocardial infarction, which was confirmed by elevated troponin I and creatine kinase levels. The patient's circulatory dynamics did not improve on medication, and he died on day 16.ConclusionsWe report the case of a patient with severe COVID-19 who died from an exacerbation of myocardial injury. Clinicians should not only evaluate respiration but also assess the heart by performing a 12-lead ECG, echocardiogram, and myocardial injury marker examination. Together, these tools can help predict which patients will develop severe COVID-19.     

Additional electrocardiographic leads in the ED chest pain patient: right ventricular and posterior leads

In the evaluation of the patient with chest pain, the 12-lead electro cardiogram is a less-than-(ECG) perfect indicator of acute myocardial infarction (AMI), particularly when used early in the course of the acute ischemic event; this relative insensitivity for AMI results from many different issues, including a less-than-optimal imaging of certain areas of the heart. It has been suggested that the sensitivity of the 12-lead ECG can be improved if 3 additional body surface leads are used in selected individuals. Acute posterior (PMI) and right ventricular myocardial infarctions are likely to be underdiagnosed, because the standard lead placement of the 12-lead ECG does not allow these areas to be assessed directly. Additional leads frequently used include leads V(8) and V(9), which image the posterior wall of the left ventricle, and lead V(4R), which reflects the status of the right ventricle. The standard ECG coupled with these additional leads constitutes the 15-lead ECG, the most frequently used additional lead ECG in clinical practice. The use of the additional leads might not only confirm the presence of AMI, but also provide a more accurate reflection of the true extent of myocardial damage.     

Detection of acute myocardial infarction using the 12-lead ECG plus inverted leads versus the 16-lead ECG (with additional posterior and right-sided chest electrodes)

BACKGROUND: The electrocardiographic (ECG) diagnosis of acute myocardial infarction (MI) should be improved. This might be done either by regarding all 24 aspects (both positive and negative leads), or a subset hereof (e.g. 19-lead ECG), of the conventional 12-lead ECG or by using additional electrodes. The purpose of this study was to investigate the accuracy of the different ECG methods in diagnosing acute ST-elevation MI. METHODS: The study population consisted of 479 patients admitted to Lund University Hospital with acute chest pain. One conventional ECG plus leads V4R, V5R, V8 and V9 were recorded for each patient within 24 h of admittance. Biochemical markers were used as the 'gold standard' for diagnosis of MI. We measured ST-segment elevations in the 12-, 16- and 24-lead postadmission ECGs as well as in the 12-, 19- and 24-lead admission ECGs. RESULTS: The sensitivity for detecting acute MI was 28% for the postadmission 12-lead ECG, 33% for the 16-lead ECG and 37% for the 24-lead ECG. The specificities were 97%, 93% and 95%, respectively. For admission ECGs, the sensitivity was 33% for the 12-lead ECG, 45% for the 19-lead ECG and 49% for the 24-lead ECG, with specificities of 97%, 96% and 94%, respectively. CONCLUSIONS: The sensitivity for detecting acute MI was higher for the 16-, 19- and 24-lead ECGs than for the conventional 12-lead ECGs. Their specificity, however, was slightly lower. If increased sensitivity for detecting MI is desired, the 24-lead or 19-lead should be used as no additional electrodes are required.     

SCREENING FOR ACUTE MYOCARDIAL INFARCTION IN ELDERLY PATIENTS WITH COLLAPSE,CONFUSION AND FALLS

Falls, collapse and confusion are frequent causes of admission to hospital in the elderly, and myocardial infarction (Ml) can present atypically. The study was designed to assess the incidence of Ml in this group of patients and provide information on the value of screening methods. A total of 142 elderly patients with a mean age of 83 years (range 76-99) were admitted with unexplained collapse, confusion or falls. Serial ECGs and cardiac enzymes were performed. Eighty-two patients (59%) had normal ECGs; of these, 80 (98%) had normal or non-significantly elevated cardiac enzymes; 72/108 patients without chest pain had normal ECGs compared with 10/32 who had chest pain (p<0.01). Cardiac enzymes were elevated in 5/108 without chest pain and 10/32 with chest pain (p<0.01). Thirty-two (23%) had chest pain, 14 (10%) had an acute Ml. In those presenting with chest pain, 32% had an Ml, compared with only 1.9% of those without chest pain (p<0.01); 18% of patients with an initially abnormal ECG had an Ml compared with only 5% of those with a normal ECG (p=0.02). None of the patients with a normal ECG who were free of chest pain were subsequently proven to have an Ml. Cardiac enzymes are often non-specifically elevated in this group of patients due to muscle injury. The incidence of Ml is low in patients without chest pain and we would not advocate routine screening with serial cardiac enzymes, unless there is chest pain or an abnormal 12-lead ECG on admission.     

直立不耐受儿童直立倾斜试验的性别和年龄差异

目的 探讨直立不耐受(OI)儿童直立倾斜试验(HUTT)的性别和年龄差异.方法 2004-01～2009-06在中南大学湘雅二医院儿童晕厥专科门诊就诊或住院的具有不明原因晕厥、头晕、胸闷、胸痛或心悸等OI症状的儿童728例,年龄3～17 岁[平均(10.67±2.85)岁],男388例,女340例.其中＜12岁416例,年龄3～11岁[平均(8.69±1.86)岁];≥12岁312例,年龄12～17岁[平均(13.30±1.50)岁].经详细询问病史、体格检查、心脏X线、超声心动图、常规12导联心电图、脑电图、头颅CT、血液生化(空腹血糖、心肌肌钙蛋白I)等排除器质性心脏病及其他疾病后行HUTT检查.结果 ①HUTT阳性率:60.71%(442/728),女性高于男性(P<0.01);≥12岁组高于＜12岁组(P<0.01).HUTT阳性率在＜12岁组男性低于女性(P<0.05),≥12岁组男性与女性比较差异无统计学意义(P＞0.05),≥12岁组男性及女性分别高于＜12岁组男性及女性(P均<0.01).②HUTT类型:以血管迷走性晕厥(VVS)多见(59.95%,265/442),其次为体位性心动过速综合征(POTS,37.56%,166/442)及体位性低血压(OH,2.49%,11/442).HUTT类型分布在男性与女性之间及＜12岁组与≥12岁组之间比较差异均无统计学意义(P均＞0.05).HUTT类型分布在男性及女性＜12岁组与≥12岁组之间比较差异无统计学意义(P均＞0.05).HUTT类型分布在＜12岁组及≥12岁组男性与女性之间比较差异无统计学意义(P均＞0.05).结论 具有不明原因晕厥、头晕、胸闷、胸痛或心悸等OI症状的儿童HUTT阳性率存在性别和年龄差异,但HUTT类型分布未见明显的性别和年龄差异.     

Rizatriptan wafer–sublingual vs. placebo at the onset of acute migraine

Rizatriptan wafer is a 5HT_1B/1D agonist for use in the acute treatment of migraine. It is a freeze-fried formulation, approved for oral administration, which dissolves on the tongue and is swallowed with saliva. In this study the efficacy of sublingually administered rizatriptan 10-mg wafer was evaluated in a randomized, double-blind, placebo-controlled, out-patient study involving 39 migraineurs. Patients were instructed to treat a migraine at the onset of pain in order to evaluate time of onset of pain relief and pain relief at 1 h. The average time to onset of relief was 25 min for patients treated with rizatriptan wafer and 27 min for patients treated with placebo. At 1 h, 50% of the patients receiving rizatriptan wafer and 50% of the patients receiving placebo experienced significant relief. Implications and potential reasons for a high placebo response are discussed.     

老年人急性心肌梗死108例临床观察

目的 提高对老年人急性心肌梗死的诊断率,减少误诊率和心肌梗死危险事件的发生.方法 急性心肌梗死所有急性心肌梗死病人分为正确诊断组和误诊两组,对两组的症状、心电图特点进行率的比较.结果 误诊组中胸闷和心电图非ST段抬高的发生率分别高于正确诊断组(P＜0.01,P＜0.05).结论 老年人急性心肌梗死以胸闷为主要症状和心电图非ST段抬高,要结合病史、动态心电图和心肌酶学监测结果综合分析,及时诊断,进行危险分层评估.     

Body surface mapping vs 12-lead electrocardiography to detect ST-elevation myocardial infarction

A prospective, multicenter trial was conducted in patients with nontraumatic chest pain in 4 hospitals to determine whether an 80-lead body surface map electrocardiogram system (80-lead BSM ECG) improves detection of ST-segment elevation in acute myocardial infarction (STEMI) compared with a standard 12-lead electrocardiogram (ECG) in an emergency department (ED) setting. A trained ED or cardiology staff member (technician or nurse) recorded a 12-lead ECG and 80-lead BSM ECG from each subject at initial presentation. Serial biomarkers (total creatine kinase [CK], CK-MB, and/or troponin) were obtained according to individual hospital practice. Of the 647 patients evaluated, 589 had available biomarkers results. Eighty-lead BSM ECG improved detection of biomarker-confirmed STEMI compared with the 12-lead ECG for CK-MB–defined STEMI (100% vs 72.7%, P = .031; n = 364) or troponin-defined STEMI (92.9% vs 60.7%, P = .022; n = 225). Specificity for STEMI was high (range, 94.9%-97.1%) with no significant difference between 80-lead BSM ECG and 12-lead ECG. Right ventricular involvement complicating inferior STEMI was detected by 80-lead BSM ECG in 2 (22%) of 9 patients with CK-MB–defined MI and in 2 (22%) of 9 patients with troponin-defined MI. The infarct location missed most commonly on 12-lead ECG but detected by 80-lead BSM ECG was inferoposterior MI. We conclude that BSM using 80-lead BSM ECG is more sensitive for detection of STEMI than 12-lead ECG, while retaining similar specificity.