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The ECG is at a crossroads as to its future integration into modern medical practice. Those most interested in electrocardiography remain the old guard, whose careers evolved with this technology. They remain as enamored by the experiential mythology as by the experimental science of the ECG. Electrophysiologists, who rightly should be carrying on the torch of further ECG development, are too busy with their therapeutic invasive procedures and devices to invest much time in diagnostic decision support. Young physicians in training are too busy learning the plethora of new diagnostic modalities and treatment procedures to even become competent in ECG interpretation. Many of them only have goals to recognize an ST elevation myocardial infarction and atrial fibrillation, and to pass their board examinations. Their understanding of ST elevation myocardial infarction criteria could be easily exposed by asking them to name the contiguous pairs of standard ECG leads. A disappointing number would refer to pairs of leads that are contiguous on the ECG display such as II and III or V1 and V4, rather than the leads separated by 30° going around the surface of the heart as specified in the guidelines.1 Reimbursement provides a further counterincentive: to paraphrase George Bernard Shaw ( The Doctor’s Dilemma , 1926), “the doctor orders the test that pays the most” and that is no longer the ECG, but a panoply of imaging procedures. Examples of the experiential mythology that continue to haunt electrocardiography include the requirement for contiguous or adjacent leads instead of a single lead for fulfilling diagnostic criteria. The contiguous or adjacent lead constraint is a residual from the thick, noisy tracings from the early days of electrocardiography before high-impedance amplifiers, DC coupling, and digital processing produced the high-resolution tracings of today (Figure 1). Applying the criteria to a …

To minimize maintenance immunosuppression in upper-extremity transplantation to favor the risk-benefit balance of this procedure.Despite favorable outcomes, broad clinical application of reconstructive transplantation is limited by the risks and side effects of multidrug immunosuppression. We present our experience with upper-extremity transplantation under a novel, donor bone marrow (BM) cell-based treatment protocol ("Pittsburgh protocol").Between March 2009 and September 2010, 5 patients received a bilateral hand (n = 2), a bilateral hand/forearm (n = 1), or a unilateral (n = 2) hand transplant. Patients were treated with alemtuzumab and methylprednisolone for induction, followed by tacrolimus monotherapy. On day 14, patients received an infusion of donor BM cells isolated from 9 vertebral bodies. Comprehensive follow-up included functional evaluation, imaging, and immunomonitoring.All patients are maintained on tacrolimus monotherapy with trough levels ranging between 4 and 12 ng/mL. Skin rejections were infrequent and reversible. Patients demonstrated sustained improvements in motor function and sensory return correlating with time after transplantation and level of amputation. Side effects included transient increase in serum creatinine, hyperglycemia managed with oral hypoglycemics, minor wound infection, and hyperuricemia but no infections. Immunomonitoring revealed transient moderate levels of donor-specific antibodies, adequate immunocompetence, and no peripheral blood chimerism. Imaging demonstrated patent vessels with only mild luminal narrowing/occlusion in 1 case. Protocol skin biopsies showed absent or minimal perivascular cellular infiltrates.Our data suggest that this BM cell-based treatment protocol is safe, is well tolerated, and allows upper-extremity transplantation using low-dose tacrolimus monotherapy.

This statement provides a concise list of diagnostic terms for ECG interpretation that can be shared by students, teachers, and readers of electrocardiography. This effort was motivated by the existence of multiple automated diagnostic code sets containing imprecise and overlapping terms. An intended outcome of this statement list is greater uniformity of ECG diagnosis and a resultant improvement in patient care. The lexicon includes primary diagnostic statements, secondary diagnostic statements, modifiers, and statements for the comparison of ECGs. This diagnostic lexicon should be reviewed and updated periodically.

The purpose of this study was to evaluate the ability of Automated Facial Image Analysis (AFA) to detect changes in facial motion after Botox injections in patients with facial nerve disorders accompanied by abnormal muscle activity. Eight subjects received Botox for oral to ocular synkinesis (n = 6), ocular to oral synkinesis (n = 1), and/or depressor anguli oris overactivity (n = 3). Subjects were video-recorded during 2 directed facial action tasks before and after Botox treatment. AFA measurement and Facial Grading System (FGS) scores were used to evaluate the effects of Botox. After Botox, AFA detected a decrease in abnormal movements of the eyelids in all patients with oral to ocular synkinesis, a decrease in oral commissure movement for the patients with ocular to oral synkinesis, and an increase in oral commissure movement in all patients with depressor overactivity. The FGS scores failed to demonstrate any change in facial movement for the case of ocular to oral synkinesis and for 2 cases of depressor overactivity. AFA enables recognition of subtle changes in facial movement that may not be adequately measured by observer based ratings of facial function.

The ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG provides an opportunity to describe location and extent of infarction expressed as pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) walls has varied over time,1–7 although the most currently accepted terms by electrocardiographists have been anterior , septal , lateral , and inferior .8–15 However, terminology has been complicated by use of posterior to refer to either the basal lateral or the basal inferior wall (see below). On the basis of correlations with the postmortem anatomic gold standard reported >50 years ago16 and confirmed later,17,18 the presence of abnormal Q waves in leads V1 and V2 was related to septal wall MI; in V3 and V4 to anterior wall MI; in V5 and V6, I, and aVL to lateral wall MI (I, aVL high lateral; V5 and V6, low lateral); and in II, III, and aVF to inferior wall MI. The presence of abnormally increased R waves in V1 and V2 as a mirror image of Q waves in posterior leads was called a posterior wall infarction . Although similar considerations may be applied for ECG location of ST-segment deviation, this report focuses only on ECG localization of the QRS-complex abnormalities indicative of established MI as depicted by cardiac magnetic resonance (CMR) imaging. Although attempts to standardize the terminology applied to the LV walls have been reported,19,20 differences persist among the terms used by anatomists, pathologists, electrocardiographists, cardiac imagers, and clinicians. However, the pathologist’s view of infarcted myocardium lacks insights into the in vivo positioning of the LV walls. CMR imaging with delayed contrast enhancement (CE-CMR) has emerged as a new anatomic …

BACKGROUND Delay in treatment of patients with ST-elevation acute myocardial infarction (STEMI) has an adverse effect on patient outcomes. Limited data are available on the effectiveness of hospital care improvement strategies (HCIS) to reduce time to reperfusion by percutaneous coronary intervention (PCI). This study evaluated the combined effect of HCIS implementation to reduce door-to-balloon time in patients with STEMI. METHODS Retrospective chart review was done for 95 consecutive patients with STEMI who underwent PCI at Charleston Area Medical Center. Patients with non-STEMI and patients transferred from other medical centers were excluded. Door-to-balloon time was defined as time from emergency department arrival to first PCI balloon inflation. A program of 3 HCIS was implemented: 1) a fast-track catheterization laboratory protocol, 2) feedback to cardiologists on their treatment times, and 3) a weekday 24-hour inhouse catheterization laboratory team. Patients were separated into groups before (n = 46), during (n = 18), and after (n = 31) HCIS implementation. RESULTS Mean age was 60.3 +/- 13 years and 74% were male. The majority (64%) arrived by ambulance; 29% had a prehospital electrocardiogram done. Most patients presented during the day (68%) on weekdays (75%). Symptom onset-to-door time was 289 +/- 393 minutes. No significant differences were found between the groups for these variables. Door-to-PCI time in minutes was reduced in the group after versus the group before HCIS implementation (94.3 +/- 37 vs 133.5 +/- 53; P < 0.0001). CONCLUSION Implementation of HCIS shortened door-to-PCI time for patients with STEMI by 39.2 +/- 10 minutes. Thus, HCIS may be effective in improving patient outcomes.

SUMMARY: Percutaneous transluminal coronary angioplasty provides an excellent opportunity to investigate the location and quantity of hypoperfusion during sudden complete occlusion of one of the major coronary arteries. Thirty-five patients referred for elective percutaneous transluminal coronary angioplasty were injected intravenously with 99mTc-sestamibi during balloon inflation. To visualize and quantify the hypoperfused region, a map of perfusion was constructed from that occlusion study and from the control study performed on the following day. Patients were divided into groups according to proximal or distal occlusion within each of the three coronary arteries. The region of myocardium supplied by each coronary artery varied in location and extended outside the typical borders for all arteries, but most prominently for the left circumflex coronary artery. The quantities of hypoperfusion varied within each artery group, but the average hypoperfusion was greater for the left anterior descending coronary artery than for either the right coronary artery or the left circumflex coronary artery. It is concluded that the quantities of hypoperfusion were highly variable within each artery group. Occlusion of the left anterior descending coronary artery was associated with the largest ischaemic region. The area of hypoperfusion extended outside the typical borders, most prominently for the left circumflex coronary artery. (Less)

Background Myocardial salvage is most likely to occur when thrombolytic therapy is administered within 4 to 6 hours of the onset of symptoms of myocardial infarction. The impact of delays within this early time period on final myocardial infarct size are unknown. The purpose of this study was to quantitate the relation between final myocardial infarct size and duration of symptoms before initiation of thrombolytic therapy in patients treated within 6 hours of symptom onset. Methods and Results The findings from patients in four prospective randomized trials of thrombolytic therapy were combined for analysis. The study population consisted of 432 patients presenting within 6 hours of onset of symptoms of first acute myocardial infarction who met ECG criteria that allowed estimation of myocardial area at risk before treatment with thrombolytic therapy and who had thallium-201 myocardial infarct–size measurements performed several weeks after infarction. ECG analysis revealed no difference in myocardium at risk for infarction as a function of duration of symptoms before initiation of thrombolytic therapy. In contrast, univariate and multivariate analysis showed that final infarct size was highly dependent on duration of symptoms before initiation of therapy. Each 30-minute increase in symptom duration before thrombolytic therapy was associated with an increase in infarct size of 1% of the myocardium. Final infarct size in patients treated 4 to 6 hours after symptom onset was indistinguishable from patients who did not receive thrombolytic therapy. Conclusions These findings suggest that for patients treated within 4 to 6 hours of the onset of symptoms, there is a progressive decline in the extent of myocardium salvaged as the duration of symptoms before therapy increases. These results support efforts to minimize the time delay between symptom onset and initiation of reperfusion therapy in all eligible patients.

Background : Myocardial scarring from infarction (MI) or nonischemic fibrosis forms an arrhythmogenic substrate. The Selvester QRS-score estimates MI size by quantifying changes in Q-, R- and S-wave durations, amplitudes and morphologies from the 12-lead electrocardiogram (ECG). It provides 32 possible points with each point reflecting scarring of 3% of the left ventricle (LV). Although QRS scoring has been extensively validated for estimating MI scar size in the absence of ECG confounders, it has not been validated in patients with left ventricular hypertrophy (LVH), fascicular/bundle branch blocks or nonischemic scar. We assessed the hypotheses that QRS-scores (modified for each conduction type) correctly identify and quantify both ischemic and nonischemic scar as compared to the reference standard of Cardiac Magnetic Resonance - Late Gadolinium Enhancement (CMR-LGE) and QRS-estimated scar size is associated with inducible sustained monomorphic ventricular tachycardia (MVT) during electrophysiologic (EP) testing. Methods and Results: A prospective 162 patient cohort with LV dysfunction (95 ischemic, 67 nonischemic) received 12-lead ECG and CMR-LGE before defibrillator (ICD) implantation for primary prevention of sudden cardiac death. QRS-scores correctly diagnosed CMR-scar presence with receiver operating characteristics (ROC) area under the curve (AUC)=0.91 and correlation for scar quantification of r=0.74, p Conclusions : Compared to CMR, QRS-scores identify and quantify MI and nonischemic scar despite ECG confounders. Higher QRS-estimated scar size is associated with increased arrhythmogenic potential and warrants further study as a risk-stratifying tool for patients with left ventricular dysfunction.

Background: The potential for salvage of jeopardized myocardium during coronary occlusion decreases as the duration of persistent ischemia is prolonged. Thus, it is important to be able to assess the acuteness of ischemia as a patient presents with signs of acute coronary syndrome. The aim of this study was to compare ECG estimate of ischemic acuteness and time from pain onset for predicting myocardial salvage in patients with first-time myocardial infarction (MI). Methods: Thirteen patients with acutely revascularized first-time MI were studied. All patients had 99mTc tetrofosmin injected and an ECG recorded prior to the PCI. TIMI III flow was obtained in all patients. Single photon emission computed tomography (SPECT) was undertaken within 3 hours of the PCI to assess the myocardium at risk (MaR). Delayed contrast-enhanced magnetic resonance imaging (DE-MRI) was performed 1 week after admission for assessment of infarct size (IS) and infarct transmurality (IT). A salvage index was calculated as (MaR-IS)/MaR. The acuteness of ischemia was estimated both from patient history and from the Anderson-Wilkins (AW) acuteness score of the pre-PCI ECG. Results: The figure shows the relationship between time of symptom onset and salvage index (A) and IT (C) as well as the relationship between AW acuteness score and salvage index (B) and IT (D). The time of symptom onset did not correlate with salvage index or IT. The AW acuteness score, however, showed a significant relationship with both salvage index and IT. Conclusions: The initial ECG changes are superior to time from symptom onset to PCI for predicting myocardial salvage and IT in patients undergoing PCI of first-time MI.

This report represents our experience with 522 consecutive patients with acute myocardial infarction admitted directly to the Duke Coronary Care Unit. Fifty items of information were used to characterize the patients, their hospital course and follow-up. Serious complications included death, ventricular tachycardia or fibrillation, second- or third-degree heart block, pulmonary edema, cardiogenic shock, persistent sinus tachycardia or hypotension, atrial flutter or fibrillation, and extension of infarction. Forty-nine percent of the patients (252 of 522) experienced a serious complication. All patients who experienced any serious complications had at least one of the above during the first four days of hospitalization. Patients who survived through day 4 were subgrouped on the basis of the occurrence (complicated) or lack of occurrence (uncomplicated) of the above on day 5. Complicated patients had a subsequent hospital mortality of 14% and an incidence of late serious complications of 51%. Patients who were uncomplicated through day 4 had a subsequent hospital mortality of zero and an incidence of late serious complications of zero. These data suggest that it would be feasible and ethically justified to conduct a prospective clinical trial of early discharge (7th day) in patients who meet the above criteria for uncomplicated. The potential economic savings through earlier discharge in uncomplicated patients are of major significance.

This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single well-circumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated. Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVf in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads. This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy.

We evaluated a simplified version of a previously developed QRS scoring system for estimating infarct size using observations of Q- and R-wave durations and R/Q and R/S amplitude ratios in the standard 12-lead ECG. Groups of subjects with a minimal likelihood of having myocardial infarcts and minimal likelihood of having common noninfarction sources of QRS modification were studied to establish the specificity of each of the 37 criteria. Only two criteria required modification to achieve 95% specificity. These 37 criteria form the basis of a 29-point QRS scoring system. A 98% specificity was achieved when a score of more than 2 points was required to identify a myocardial infarct. Fifty patients were studied to determine the intra- and interobserver agreement with this scoring system. Each criterion achieved at least 91% intra- and interobserver agreement. These impressive levels of specificity and observer agreement must be matched by high sensitivity of the scoring system and a good correlation between the point score and infarct size in patients with proven infarcts if the point score is to be useful for detecting and sizing infarcts. Sensitivity and correlation between point score and infarct size are evaluated in later studies in this series. The standard ECG is inexpensive and can be obtained repetitively and noninvasively; its QRS complex may be an important means of estimating the size, presence and location of myocardial infarcts.

Frank-lead vectorcardiograms (VCGs) and standard 12-lead electrocardiograms (ECGs) were analyzed to develop simple, linear, quantitative criteria for the diagnosis of right ventricular hypertrophy (RVH). The study subjects included a population with a definite RVH (84 patients with mitral stenosis proved by cardiac catheterization and pulmonary arterial systolic pressure > 40 mm Hg) and a population with minimal likelihood of RVH (173 young, healthy volunteers and 151 normal subjects proved by cardiac catheterization). VCGs were evaluated to identify criteria that provided maximum sensitivity and at least a 95% specificity: the maximum QRS magnitude had to be < 1.8 mV and either (1) the amplitude at -45 degrees (transverse plane) had to be < 0.3 mV or (2) the maximum anterior amplitude plus the maximum rightward amplitude minus the amplitude at -45 degrees must be greater than or equal to 0.5 mV. Application of these criteria achieved 60% (50 of 84) sensitivity in patients with RVH, similar to that for previous VCG criteria but significantly better (p < 0.01) than the best sensitivity with any ECG criteria (27%, 23 of 84). The specificity of the proposed criteria was 96% (310 of 324), significantly better (p < 0.001) than the 78% specificity (252 of 324) of existing VCG criteria. Thus, linear measurements of the QRS complex displayed on the VCG identify 60% of patients with moderate-to-severe RVH and falsely indicate RVH in only 4% of normal subjects.

Two hundred and five patients who received a total of 247 electrode systems-129 transvenous, 68 transmediastinal and 50 transthoracic-are compared after complete uniform two-year follow-up. The transvenous patients had low hospital morbidity (19%) and short hospital stays (75% ≤ 8 days) but a high incidence of electrode failure by 24 months (38%). The transmediastinal and transthoracic patients had more hospital complications (35% and 34%) and longer periods of hospitalization (57% and 70% > 8 days) but fewer instances of failure by 24 months (16% and 11%). Most transvenous electrode failures were secondary to dislodgement. Transmediastinal right epicardial electrodes had the unique problem of threshold elevation and failure between six and 12 months after implantation as well as a high incidence of sudden death in this same period. Although the high incidence of endocardial electrode instability dictates the need for an alternative approach to permanent pacing, the failure of the transmediastinal approach to significantly alter postoperative morbidity (as compared with transthoracic electrodes) and the incidence of threshold elevation remote from right ventricular implantation suggest that limitation of thoracotomy (via the transmediastinal approach) should not take precedence over left ventricular implantation. Development of electrodes which would provide more permanent low resistance fixation to right ventricular endocardium or epicardium may be necessary before the transthoracic approach can be abandoned.

The indication for prophylactic temporary and permanent pacing during acute myocardial infarction (MI) complicated by bundle branch block is high risk of progression via a Type II pattern to second or third degree (high degree) AV block during hospitalization or follow-up. In this study, determinants of high degree AV block during hospitalization and sudden death or recurrent high degree block during the first year of follow-up were examined in 432 patients with MI and bundle branch block. Timing of onset of bundle branch block, the involved fascicles, and the PR interval were examined as determinants of risk of progression to high degree AV block during MI. At highest risk were 186 patients with blocks involving the right bundle and at least one fascicle of the left bundle which were not documented on prior electrocardiograms. Risk was similar with (38%) or without (31%) accompanying first degree AV block. Patients with transient high degree AV block during MI had a 28% incidence of sudden death or recurrent high degree block during the first year of follow-up. Patients not continuously paced had a higher incidence of sudden death or recurrent high degree block than patients continuously paced (65% vs 10%, P less than 0.001). Sudden death during follow-up also occurred in 13% of patients without high degree block during MI. A subgroup with 1) documented prior MI, 2) anterior or indeterminant acute MI, and 3) no symptoms of cardiac failure had a 35% risk of sudden death. The role of permanent pacing in this group is unknown. Thus, patients at high risk of high degree AV block should receive prophylactic temporary pacing. Patients who survive high degree block with MI should receive temporary and then permanent pacing. Patients without high degree AV block during MI who nervertheless have a high risk of sudden death may benefit from permanent pacing.

Vectorcardiograms (VCG) from a consecutive group of 77 patients with significant aortic valve disease were analyzed. All of the patients had complete left and right heart catheterization with normal coronary arteriograms and normal left ventricular contraction. Thirty-five (46%) patients met VCG criteria for anterior myocardial infarction (AMI-35%) and/or inferior myocardial infarction (IMI-14%). This was a significant increase in false positive diagnosis for both criteria compared to a group of 200 normal volunteers under age 30 and 100 patients with normal hearts by cardiac catheterization (P less than 0.01). It was found that if the VCG diagnosis of myocardial infarction was deferred when the maximal transverse plane magnitude was greater than 1.9 mV, the incidence of AMI false positive diagnosis decreased to 3% and the incidence of IMI false positive diagnosis decreased to 1%. The same rule was applied to the aortic valve disease cohort, a group of 124 patients with documented AMI and a group of 158 patients with IMI. This decreased the sensitivity of the AMI criteria from 93 to 83% and of the IMI criteria from 85 to 77%. The increase in average performance was statistically significant fro the AMI criteria (P less than 0.05) but not for the IMI criteria.

Ventriculograms made 9-15 months after surgery in 48 patients with normal preoperative apical contraction were reviewed to determine the influence of apical venting on apical wall motion in patients undergoing coronary bypass surgery. After interpretation of postoperative apical wall motion, the patients were subdivided into two groups. One group consisted of 34 patients who were vented by inserting a catheter through the apex of the left ventricle and the second group included 14 patients in whom no transventricular vent was made. The two groups were similar clinically and hemodynamically before surgery, and the surgical procedures were similar with the exception of vent site. Following surgery, incidences of graft patency and antegrade flow to the apex were also similar. Nineteen (56%) patients in the apically vented group had apical dyskinesia or akinesia observed on the postoperative ventriculogram while none of the patients who were not apically vented had these findings. None of the patients with apical dyskinesia or akinesia had congestive heart failure following surgery. The postoperative ventriculograms of 12 patients with mitral stenosis who underwent valvulotomy by inserting a Tubbs dilator through the apex were also analyzed. Only one patient (8.5%) had apical dyskinesia or akinesia. Since the patients with mitral stenosis probably did not have significant coronary artery disease, it is possible that the combination of the apical vent and ischemic heart disease was responsible for the focal contraction abnormalities observed.

The electrocardiograms of 538 patients with acute myocardial infarction were searched to identify all instances of atrioventricular (A-V) and intraventricular (I-V) conduction disturbances. Data concerning mode of therapy and clinical complications were obtained by review of the record. These variables were then analyzed for significance in relation to the development of type II A-V block acutely and syncope or sudden death during the first year of follow-up. The most accurate predictor for both these events was the status of A-V conduction in combination with the status of I-V conduction. At highest risk (50%) for type II progression were patients with acute adjacent fascicular block plus P-R prolongation, i.e., left anterior hemiblock plus right bundle-branch block (RBBB), or left bundle-branch block (LBBB), or patients with acute nonadjacent fascicular block, i.e., RBBB plus left posterior hemiblock or alternating bundle-branch block. The nonpaced survivors from this same group, plus any other patients with transient type II progression, were also at high risk (45%) for syncope or sudden death in follow-up. No syncope or sudden death has occurred in seven patients with type II progression discharged with a pacemaker. All other patients were at lower risk for these acute and chronic complications. Thus, the electrocardiogram in acute myocardial infarction can identify a high-risk group for acute type II progression in whom prophylactic pacer insertion may be beneficial. Similarly, the electrocardiogram can identify a high-risk group for syncope or sudden death in follow-up and implicates progression to higher degrees of A-V block as an important pathophysiologic mechanism.The possible role of permanent pacemaker therapy in preventing syncope or sudden death in this high-risk group is also suggested.

These experiments were designed to examine the role of excitation of intracardiac nerves in the response to countershock with either alternating current (ac) or direct current (dc). Studies were performed on intact anesthetized dogs and on isolated perfused hearts. In intact dogs a-c and d-c countershock produced transient sinus arrest and an increase in myocardial contractile force. Sinus arrest could be prevented with atropine, and the positive inotropic response could be prevented with propranolol or prior surgical denervation of the heart. In isolated hearts, a-c and d-c countershock produced sinus arrest which could be prevented with atropine or hemicholinium-3. Alternating-, but not direct-, current countershock increased contractile force of the isolated heart. The inotropic response to ac could be blocked with propranolol and was absent in hearts removed from dogs which had undergone prior cardiac denervation. Both a-c and d-c countershock produced a decrease in coronary vascular resistance which could be prevented with atropine. Cholinergic responses to countershock persisted after surgical denervation of the heart. These observations provide evidence for excitation of intracardiac cholinergic and adrenergic nerves by countershock. Direct-current countershock excites cardiac sympathetic nerves in intact dogs, but not in isolated hearts. Intracardiac cholinergic nerves persist after surgical denervation of the heart.

Routine enzymatic and electrocardiographic diagnosis of postoperative acute myocardial infarction (AMI) is frequently inconclusive. The detection and quantitation of isoenzymes of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), especially the cardiac-specific CPK-MB isoenzyme, have allowed earlier recognition of AMI in nonsurgical patients. Serial monitoring with these methods has been utilized during the postoperative period in 20 noncardiac surgical patients and 100 patients undergoing coronary artery bypass grafting (CABG). In the noncardiac surgery group, both isoenzymes were accurate in diagnosing AMI in the early postoperative period. Of the 100 patients in the CABG group, CPK-MB appearance in 21 correlated with AMI by electrocardiogram. The absence of CPK-MB postoperatively in 49 patients permitted a 73% incidence of new ECG abnormalities to be effectively resolved. Autopsy confirmation of AMI was obtained in two patients with nondiagnostic ECG, but with elevated CPK-MB. The elevated CPK-MB without ECG evidence of AMI in the remaining patients could possibly be explained by varying degrees of myocardial damage produced by intraoperative cardiac manipulation. These data demonstrate the value and sensitivity of CPK-MB isoenzyme determinations in the early recognition of postoperative acute myocardial infarction.