Cardioprotective properties of opioid receptor agonists in rats with stress-induced cardiac injury.

The objectives of this study were to investigate the role of endogenous opioids in the mediation of stress-induced cardiomyopathy (SIC), and to evaluate which opioid receptors regulate heart resistance to immobilization stress. Wistar rats were subjected to 24 h immobilization stress. Stress-induced heart injury was assessed by 99mTc-pyrophosphate accumulation in the heart. The opioid receptor (OR) antagonists (naltrexone, NxMB - naltrexone methyl bromide, MR 2266, ICI 174.864) and agonists (DALDA, DAMGO, DSLET, U-50,488) were administered intraperitoneally prior to immobilization and 12 h after the start of stress. In addition, the selective micro OR agonists PL017 and DAMGO were administered intracerebroventricularly prior to stress. Finally pretreatment with guanethidine was used. Naltrexone did not alter the cardiac 99mTc-PP accumulation in stressed rats. NxMB aggravated stress-induced cardiomyopathy (P=0.005) (SIC). The selective micro OR agonist DALDA, which does not cross the blood-brain barrier, completely prevented (P=0.006) SIC. The micro OR agonist DAMGO exhibited weaker effect than DALDA. The selective delta ligand (DSLET) and kappa OR ligand (U-50,488) did not alter stress-induced 99mTc-pyrophosphate accumulation in the heart. Intracerebroventricular administration of the micro OR agonists aggravated SIC. Pretreatment with guanethidine abolished this effect (P=0.01). Guanethidine alone exhibited cardioprotective properties. A stimulation of central micro OR promotes an appearance of SIC. In contrast, stimulation of peripheral micro OR contributes to an increase in cardiac tolerance to stress.

Electrocardiogram in apical hypertrophic cardiomyopathy with a speculation as to the mechanism of its features.

A variety of electrocardiogram (ECG) alterations in patients with apical hypertrophic cardiomyopathy (AHCM) have been described in the literature, but no relevant quantitative analysis has been provided; thus the objective of this communication was to review the relevant literature and using two cases of patients with AHCM, to provide such a quantitative analysis. Using PubMed to search the literature 13 studies on the ECG in patients with AHCM were identified and evaluated; also a quantitative analysis of the ECG attributes in two patients was carried out. Qualitative ECG features from the literature on patients with AHCM is discussed. Also a description of the ECG in two patients with AHCM has identified as typical features truly giant QRS complexes in the precordial leads, particularly in lead V4, with rightward superior, and posterior shift of the T-wave vector, the latter being a newly described ECG correlate of AHCM. A speculation as to the possible mechanism of the observed ECG features is included.

A critique of the new ST-segment criteria for the diagnosis of acute myocardial infarction in patients with left bundle-branch block.

BACKGROUND: Recently, electrocardiogram (ECG) criteria have been proposed for the diagnosis of acute myocardial infarction (AMI) in the presence of left bundle-branch block (LBBB). However, clinical experience indicates that such ECG changes indicative of AMI are occasionally noted in clinically stable patients with LBBB, raising concerns about the specificity of the proposed criteria. HYPOTHESIS: The aim of this study was to evaluate the frequency of ST-segment abnormalities suggestive of AMI in ambulatory patients with cardiovascular disease and chronic LBBB, who did not have an AMI. In addition, the ECG determinants of such ST-segment abnormalities were sought. METHODS: The files of all (4,193) patients followed in the outpatient cardiology clinic were reviewed to identify patients with LBBB. Electrocardiograms of these patients were evaluated as to the duration of the QRS complex, frontal QRS axis, amplitude of QRS in leads V1-V3, and the presence and magnitude of ST-segment depression (-ST) in leads V1-V3, and ST-segment elevation (+ST) in leads with predominantly positive or negative QRS complexes. Correlations of these ECG variables were carried out. RESULTS: In 124 patients with LBBB only 1 patient with -ST of 1 mm in leads V1-V3, and 1 patient with +ST of 1 mm in a predominantly positive ECG lead were found; the latter patient also had +ST of 6 mm in V3. Nine patients were detected with > or = 5 mm +ST in at least one ECG lead with predominantly negative QRS complex. Regression analysis of amplitude of +STs on corresponding QRS amplitudes in leads V1-V3 yielded Rs of 0.69, 0.68, and 0.69, all with a p value of 0.00005. A similar analysis of the amplitudes of +STs > or = 5 mm with the corresponding QRSs yielded an R = 0.76 and a p value of 0.0018. CONCLUSIONS: Thus, recently proposed ST-segment criteria for the diagnosis of AMI in patients with LBBB are appropriate. However, stable > or = 5 mm +STs are occasionally found in leads with predominantly negative QRS complexes, particularly of large amplitude (mean value 46.0, range [28.0-71.0] mm) in the absence of AMI. In such patients presenting with symptoms suggestive of AMI, further non-ECG confirmation of probable underlying AMI should be sought.

Anasarca-mediated attenuation of the amplitude of electrocardiogram complexes: a description of a heretofore unrecognized phenomenon.

OBJECTIVES: The relationship between the changes of weight (WT) and electrocardiogram (ECG) QRS amplitude in patients with anasarca (AN) was evaluated. BACKGROUND: Attenuation of the ECG voltage occurs as the electrical current spreads from the epicardium to the body surface. The voltage registered is a function of the cardiac potentials, the electrical resistivities of the intervening tissues and the orientation of the ECG leads with respect to the direction of propagation of excitation. Lung congestion and pericardial and pleural effusions can cause attenuation in the ECG potentials; additionally, a similar change was recently observed in patients with AN. METHODS: A prospective study of this phenomenon in 28 patients with a critical illness was carried out. Electrocardiograms and patients' WTs were recorded daily. Pericardial effusions were excluded by serial echocardiograms. The sums of the amplitude of QRS complexes from the 12 ECG leads (Sigma QRS) were correlated with the corresponding WTs. Intracardiac ECGs, done in three patients, were correlated with surface ECGs. RESULTS: Admission WT was 148.9 +/- 37.8 lbs, and it peaked to 197.8 +/- 52.3 lbs (p = 0.0005). Admission Sigma QRS was 120.2 +/- 41.6 mm and dropped to 54.8 +/- 26.9 mm at time of peak WT (p = 0.0005). Regression of Sigma QRS on WT revealed an r = 0.61 and a p = 0.0005. Subsequent WT loss in 13 patients (from 219.0 +/- 40.7 lbs to 179.5 +/- 41.7 lbs, p = 0.001) led to an increase of Sigma QRS from 53.5 +/- 24.5 mm to 86.8 +/- 38.2 mm (p = 0.001). Intracardiac ECGs remained stable, while surface ECGs changed with perturbations of WT. CONCLUSIONS: Attenuation of ECG voltage in patients with AN correlates with WT gain, and it can be attributed to a shunting of the cardiac potentials due to the low resistance of the AN fluid.

Unusual ECG responses to exercise stress testing.

We describe the case of a patient with coronary artery disease who developed transient ST-segment depression, right bundle branch block (RBBB), left anterior hemiblock, ST-segment elevation +ST), and "giant" T-waves in her electrocardiogram (ECG), an assortment of ECG patterns heretofore unreported in conjunction with exercise stress testing (EST). The amplitude of the +ST was modulated by the superimposed RBBB, as was shown by its augmentation after the abrupt disappearance of RBBB. Following recession of the latter "giant" T-waves, which usually are encountered in the hyperacute phase of myocardial infarction, developed and persisted late in the recovery period. Cardiac enzymes after EST were negative, and arteriography revealed a stenotic left anterior descending coronary artery. The present case indicates that a variety of ECG expressions of severe transmural ischemia or myocardial infarction can also be manifest in the course of EST; this also suggests a common pathophysiological mechanism in severe EST-triggered ischemia and the early phase of myocardial infarction.

Diagnosis of myocardial infarction-induced ventricular aneurysm in the presence of complete left bundle branch block.

An analysis of the 4,196 files of our Cardiology Clinic cohort showed 128 patients with a complete left bundle branch block (LBBB) in their electrocardiograms (ECGs). Of these patients, 27 had suffered a myocardial infarction in the past and had been found to have a ventricular aneurysm (VA), documented by > or = 1 of several noninvasive and invasive diagnostic methods. Five of these 27 patients had stable ST-segment elevation in > or = 1 of left precordial ECG leads, with predominantly positive QRS complexes (an ECG criterion for the diagnosis of VA in the presence of LBBB, which we have recently described). The sensitivity of this ECG criterion for the diagnosis of VA was 18.5%, and the specificity was 100%. The frequency of distribution of VA in the septal, and even more, apical myocardial regions was higher in the patients with a positive ECG diagnosis of VA, than in the patients with a negative one (P = .049, and P = .009, correspondingly). The number of myocardial territories involved with a VA was not different in the 2 subgroups (P =.325). Pathophysiologically, this ECG alteration diagnostic of VA represents a superimposition of the primary ST-segment elevation due to the VA, on the expected secondary ST-segment depression due to the LBBB, and represents a summation effect.

Giant R-waves in a patient with an acute inferior myocardial infarction.

We describe a case of a male patient with "giant" R-waves (GRWs) in association with an acute inferior myocardial infarction (MI). Such electrocardiogram (ECG) pattern has been associated heretofore with the hyperacute phase of an anterior MI, and unstable, and variant angina, although it is found in illustrations of many previous publications in conjunction with inferior MI. The GRWs, along with ST-segment elevations, were noted transiently in the inferior ECG leads, early in the clinical course of our patient. Subsequent evolution of the ECG revealed classic appearances for an inferior MI. Cardiac enzymes, and thallium-201 myocardial perfusion scintigraphy revealed evidence for inferiorly-located myocardial necrosis. Coronary arteriography showed stenosis of the right coronary artery, for which the patient underwent an uneventful angioplasty and "stenting" of the culprit vessel. The pathophysiology of the syndrome of GRWs is briefly discussed.

Admission serum potassium in patients with acute myocardial infarction: its correlates and value as a determinant of in-hospital outcome.

STUDY OBJECTIVES: Although controversial, hypokalemia (LK) in patients with acute myocardial infarction (MI) is thought to predict increased in-hospital morbidity, particularly cardiac arrhythmias, and mortality. Also, the mechanism of low serum potassium in the setting of MI has not been delineated. We evaluated the frequency, attributes, and outcome, and speculated on the mechanism of LK in patients with MI. DESIGN: This was a prospective cross-sectional study of 517 consecutive patients with MI admitted to the coronary care unit (CCU). Serum potassium was measured in the emergency department and repeatedly thereafter throughout hospitalization, and was used in the analysis, along with a large array of clinical and laboratory variables. RESULTS: The patients were allocated to a LK and a normokalemic (NK) cohort, based on the emergency department serum potassium measurement. The 41 patients with LK (3.16+/-0.24 mEq/L; 7.9% of total) were comparable on admission in their baseline assessment to the 476 patients with normal serum potassium (4.28+/-0.56 mEq/L), except for lower emergency department magnesium (1.48+/-0.15 mg/dL vs. 1.96+/-0.26 mg/dL; p = 0.0005) and earlier presentation after onset of symptoms (3.0+/-4.1 h vs. 4.4+/- 6.2 h; p = 0.05). There was a poor correlation between serum potassium and magnesium on admission (r = 0.14). Peak creatine kinase (CK) and myocardial isomer of CK were higher in the LK patients (3,870+/-3, 840 IU/L vs. 2,359+/-2,653 IU/L [p = 0.018] and 358+/-312 IU/L vs. 228 +/- 258 IU/L [p = 0.013], respectively). Management of the two cohorts was the same, except for a higher rate of use of magnesium (14.6% vs. 4.6%; p = 0.007), serum potassium supplements (90.2% vs 43. 1%; p = 0.000005), and antiarrhythmic drugs (78.0% vs 50.4%; p = 0. 0007) in the LK patients. No difference was detected between the LK and NK patients in total mortality (24.4% vs. 18.3%; p = 0.34), cardiac mortality (17.1% vs. 15.3%; p = 0.52), atrial fibrillation (14.6% vs 13.9%; p = 0.89), and ventricular tachycardia (22.0% vs. 16.0%; p = 0.32), but ventricular fibrillation (VF) occurred more often (24.4% vs 13.0%; p = 0.04) in the LK patients. However, proportions of VF occurring in the emergency department, CCU, or wards in the two cohorts were not different, but they were higher during the time interval prior to emergency department admission in LK patients (17.1% vs 2.1%; p = 0.00001). CONCLUSIONS: LK is seen in approximately 8% of patients with MI in the emergency department; LK is associated with low emergency department magnesium, and low serum potassium levels in the CCU and throughout hospitalization. LK has no relationship to preadmission use of diuretics, it is associated with early presentation to the emergency department, and it is not a predictor of increased morbidity or mortality.

True-positive exercise electrocardiogram/false-negative thallium-201 scintigram: a proposal of a mechanism for the paradox.

A 72-year-old man with exertional angina had a strongly positive exercise electrocardiogram (EECG) with a negative thallium-201 myocardial perfusion scintigram (Tl). Arteriography revealed triple-vessel coronary artery disease, for which he underwent aortocoronary bypass grafting. Repeat EECG was negative, and it was again associated with a negative Tl. The false-negative Tl on the first test was felt to be due to a rare phenomenon of homogeneously distributed reversible exercise-induced myocardial ischemia, leading to a uniform radiotracer count density. The even distribution of ischemia would also be expected to render a false-negative EECG, due to electrocardiographic cancellation, and this is frequently the case. However, in the patient presented herein, we propose that the ischemic cardiac apex rendered the EECG strongly positive because its position was not opposed by an ischemic muscular region, and thus an uncancelled ischemic ST-segment vector was generated. This hypothesis is supported by our recent work showing the unique role of the ischemic apex (among all the other myocardial territories) in rendering the EECG positive.

Incomplete ECG expression of acute true posterior myocardial infarction, owing to an antecedent anterior infarction.

We present a 75-year-old man with an inferior and true posterior (TP) myocardial infarction (MI), who showed disproportionately deeper ST-segment depression (decreased ST) in the precordial electrocardiogram (ECG) leads than the ST-segment elevation (increased ST) noted in leads 2, 3, and aVF. This suggested that the precordial decreased ST was not reciprocal to the inferior increased ST, but it was indicative of TP ischemic injury. However, the precordial decreased ST, in subsequent serial ECGs, was not followed up by R waves of increasing amplitude, or tall T waves in the V1 and V2 leads, as would be expected had this been a case of evolving TP MI. Nevertheless, TP MI was confirmed by echocardiography and dipyridamole/thallium SPECT myocardial perfusion scintigraphy. These last 2 modalities also revealed evidence of an anterior (A) MI, which had indeed occurred 11 years previously, and was confirmed by a history of hospitalization, serial ECGs, and enzymatic evidence of necrosis. This incomplete ECG expression of TP MI in our patient was felt to be owing to the previous large A MI, which had long ago deprived the heart from requisite healthy myocardium opposite the recent TP MI, for generation of tall R waves or R/S ratio greater than 1 in the V1 and V2 leads. This case is presented as an example of electrical cancellation affecting the QRS complexes.