Left Ventricular Involvement Research Articles

Atrial natriuretic peptide: relation to left ventricular filling properties in patients with systemic sclerosis

To determine the relation between left ventricular filling properties and plasma atrial natriuretic peptide in systemic sclerosis, we evaluated 30 consecutive patients and 48 age- and sex-matched controls. The venous plasma atrial natriuretic peptide was measured by radio-immunoassay. Left ventricular involvement was evaluated by echocardiography and mitral regurgitation was evaluated by Doppler. The patient group had markedly elevated plasma atrial natriuretic peptide as compared to the matched controls (239.4 ± 59 vs. 178.2 ± 36 pmol/l, P < 0.0005). We found signs of impaired left ventricular filling properties among the patients, with an increase of the Doppler A-wave velocity and A E ratio. A relative reduction of early filling was found in spite of some degree of mitral regurgitation in two-thirds of the patients. The plasma atrial natriuretic peptide concentration was related to the A-wave velocity ( r = 0.44, P < 0.0005), the A E ratio ( r = 0.40, P < 0.005), and also to the degree of mitral regurgitation ( r = 0.43, P < 0.005). The relationship to the A-wave velocity remained when considering possible confounding factors. We conclude that the previously observed fibrotic process in systemic sclerosis does not prevent production and liberation of plasma atrial natriuretic peptide in relation to factors distending the left atrium, such as altered left ventricular filling properties and the presence of mitral regurgitation. However, the moderate relationships between atrial natriuretic peptide and haemodynamic variables indicate that the peptide might also be an independent indicator of cardiac involvement in systemic sclerosis.

Surgical treatment of arrhythmogenic right ventricular dysplasia: Long-term outcome

Eight male patients ranging from 15 to 51 years old (mean age, 36.3 years) underwent surgical treatment of ventricular tachycardia (VT) associated with arrhythmogenic right ventricular dysplasia. One patient had an associated left ventricular aneurysm. The earliest activation site was detected for 15 lesions, and delayed potentials were recorded during sinus rhythm in all patients. On the basis of the epicardial mapping, the origins of the VT foci in the right ventricle were resected. Cryoablation on the surrounding myocardium was performed. There were no surgical deaths or postoperative fatal complications. During long-term follow-up, there has been no recurrence of VT and no congestive heart failure in the 6 patients without left ventricular involvement. The 2 patients with LV involvement died late of either congestive heart failure or development of VT originating from the left ventricle. In conclusion, a surgical approach consisting of myocardial excision and cryocoagulation offers a curative treatment of VT associated with arrhythmogenic right ventricular dysplasia and yields excellent long-term results when the VT origin is well identified in the right ventricle.

Regional myocardial sympathetic dysinnervation in arrhythmogenic right ventricular cardiomyopathy. An analysis using 123I-meta-iodobenzylguanidine scintigraphy.

In patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), the frequent provocation of ventricular tachycardia during exercise, the sensitivity toward catecholamines, and the response toward antiarrhythmic drug regimen with antiadrenergic properties suggest an involvement of the sympathetic nervous system in arrhythmogenesis. To analyze the presence, extent, and location of impaired myocardial sympathetic innervation in ARVC, 123I-meta-iodobenzylguanidine (123I-MIBG) scintigraphy was performed in 48 patients with ARVC. For comparison, 9 patients with idiopathic ventricular tachycardia and a control group of 7 patients without heart disease were investigated. In patients with ARVC, the clinical sustained (n = 25; 52%) or nonsustained (n = 23; 48%) ventricular tachycardia originated in the right ventricular outflow tract in 38 patients (79%), whereas in the remaining 10 patients (21%), the site of origin was the apical (n = 5) or inferior (n = 5) right ventricle. In 33 patients (69%), nonsustained or sustained ventricular tachycardia was provocable by exercise (n = 28 of 48; 58%) and/or by isoproterenol infusion (n = 16 of 37; 43%), whereas programmed ventricular stimulation induced sustained or nonsustained ventricular tachycardia in 16 patients each (33% each). With 123I-MIBG scintigraphy, the right ventricle was not visible in any patient. No areas of intense 123I-MIBG uptake ("hot spots") were observed. All patients of the control group and 7 of 9 patients (78%) with idiopathic ventricular tachycardia showed a uniform tracer uptake in the left ventricle. In contrast, only 8 of 48 ARVC patients (17%) showed a homogeneous distribution of 123I-MIBG uptake, whereas 40 patients (83%) demonstrated regional reductions or defects of tracer uptake. In 3 of 48 patients (6%), the defect area was < 15%; in 21 patients (44%), it was 15% to 30%; and in 16 patients (33%), it was > 30% of the polar map area of the left ventricle (mean, 23 +/- 15%; range, 0% to 57%). In 38 of 40 patients (95%) with an abnormal 123I-MIBG scan, reduced tracer uptake was located in the basal posteroseptal left ventricle, involving the adjacent lateral wall in 10, the anterior wall in 2, and the apex in 12 patients. Only 2 patients demonstrated isolated defects of the anterior or lateral wall; one involved the apex. Perfusion abnormalities in the areas of 123I-MIBG defects were excluded by stress/redistribution 201T1 single-photon emission computed tomography scintigraphy and by normal coronary angiograms in all patients. Abnormalities in 123I-MIBG scintigraphy in patients with ARVC correlated with the site of origin of ventricular tachycardia, demonstrating a regionally reduced tracer uptake in 36 of 38 patients (95%) with right ventricular outflow tract tachycardia compared with only 4 of 10 patients (40%) with other right ventricular origins of tachycardia. There was no correlation between the results of 123I-MIBG scintigraphy and the extent of right ventricular contraction abnormalities, right ventricular ejection fraction, biopsy results, coronary anatomy, or left ventricular involvement in ARVC. In patients with ARVC, regional abnormalities of sympathetic innervation are frequent and can be demonstrated by 123I-MIBG scintigraphy. Sympathetic denervation appears to be the underlying mechanism of reduced 123I-MIBG uptake and may be related to frequent provocation of ventricular arrhythmias by exercise or catecholamine exposure in ARVC. Therefore, in patients with ARVC, the noninvasive detection of localized sympathetic denervation by 123I-MIBG imaging may have implications for the early diagnosis and for the choice of antiarrhythmic drugs in the treatment of arrhythmias.

Left Ventricular Involvement in Arrhythmogenic Right Ventricular Dysplasia by T1 -Weighted and Gd-DTPA-Enhanced Magnetic Resonance Imaging

Left ventricular involvement in arrhythmogenic right ventricular dysplasia diagnosed by magnetic resonance imaging in a 60-year-old man is reported. High-intensity signal areas in the left ventricular myocardium detected by T1-weighted magnetic resonance imaging may suggest replacement of left ventricular myocytes by fat, and those detected by gadolinium diethylamine-triamine penta-acetic acid enhanced magnetic resonance imaging may reflect disrupted myocytes or fibrous tissue.

Myocarditis as a Cause of Primary Right Ventricular Failure

Patients with cardiomyopathy secondary to inflammatory myocarditis usually present with biventricular signs and symptoms. On occasion, the disease may progress focally, with left ventricular involvement predominating. This patient had elevated neck veins, edema, and a dilated right ventricle in the absence of left ventricular abnormalities. At autopsy, diffuse, transmural fibrosis of the right ventricle was found, consistent with end-stage myocarditis, with minimal disease of the left ventricle. This case emphasizes that the clinical manifestations of myocarditis can be limited to the right ventricle and should be considered in the differential diagnosis of right ventricular failure.

Sympathetic innervation of the left ventricle is impaired in arrhythmogenic right ventricular disease

Arrhythmogenic right ventricular disease (ARVD) is a disease of unknown origin that primarily affects the right ventricle and is characterized by ventricular tachyarrhythmias which may lead to syncope and even, though rarely, sudden cardiac death. In 25 patients with ARVD, sympathetic innervation of the left ventricle was assessed by iodine-123 metaiodobenzylguanidine single photon emission tomography (123I-MIBG SPET). In addition, thallium-201 SPET was performed. The diagnosis of ARVD was made by an electrophysiological study and right and left heart catheterization including right ventricular endomyocardial biopsy. Ischaemic heart disease was excluded by coronary angiography. A group of seven patients without any evidence of heart disease served as a control group. Twenty-two of the 25 patients showed reduced uptake of 123I-MIBG. The abnormal areas were located predominantly in posterior and posteroseptal segments of the heart. No focus of increased 123I-MIBG activity could be demonstrated. No patient had signs of left ventricular involvement on left ventricular angiography. In contrast to the results of the 123I-MIBG SPET, those of 201T1 SPET were normal in 16 patients. The remaining nine patients showed areas of slight hypoperfusion not correlated with the reduced 123I-MIBG uptake. 123I-MIBG scintigraphy allows detection of left ventricular adrenergic dysinnervation in ARVD patients without morphological or functional abnormalities of the left ventricle.

Right ventricular dysplasia: a clinical and pathological study of two families with left ventricular involvement.

Right ventricular dysplasia is a heart muscle disease of unknown cause that is often familial and is anatomically characterised by adipose or fibroadipose infiltration of the right ventricular myocardium. It is generally regarded as a selective disorder of the right ventricle. To investigate the prevalence and characteristics of left ventricular involvement in two families in which at least one member had right ventricular dysplasia confirmed at necropsy. Eight patients were found to be affected by right ventricular dysplasia. In three of them this was confirmed at necropsy. Echocardiography or angiography or both showed left ventricular involvement in seven. This ranged from localised wall motion abnormalities to moderate or severe left ventricular dysfunction. The disease was progressive in four cases. At necropsy the left ventricular myocardium showed predominant fibrosis and degenerative changes of the myocardial cells. There were areas of myocardial thinning with fatty infiltration at the apex in two patients. Familial right ventricular dysplasia can be a progressive disorder that affects the left ventricle. Advanced disease may be clinically confused with dilated cardiomyopathy.

Evidence for biventricular involvement in acromegaly: a Doppler echocardiographic study

To investigate left and right ventricular involvement in acromegaly, 20 patients were studied by Doppler echocardiography. Nine of them had systemic hypertension. Right ventricular free wall thickness was significantly increased in acromegalic patients (8 +/- 2 vs 4 +/- 1 mm; P < 0.001). Left ventricular mass index was augmented both in the whole group and in the subgroup of normotensive acromegalics, as compared with normals (134 +/- 33 and 115 +/- 20 vs 80 +/- 18 g.m-2; P < 0.01). Ejection phase indices were normal in the patient group, while impaired left and right ventricular diastolic filling was found. In fact isovolumic relaxation time was prolonged (118 +/- 21 vs 78 +/- 12 ms; P < 0.001), ratio of early to late mitral (0.9 +/- 0.3 vs 1.8 +/- 0.5; P < 0.001) and tricuspid (1.0 +/- 0.2 vs 1.4 +/- 0.3; P < 0.001) flow velocities were significantly decreased as compared with controls. Superior vena cava flowmetry was also abnormal showing a marked decrease of diastolic filling wave and, consequently, of the ratio between peak diastolic and peak systolic flow velocity. No significant differences were observed between normotensive and hypertensive acromegalics, except for left ventricular mass index (115 +/- 20 vs 156 +/- 31 g.m-2; P < 0.01). These findings indicate that abnormal diastolic filling patterns of transmitral, transtricuspid, and superior vena cava flowmetry suggesting 'impaired relaxation' associated with increased left and right ventricular mass, frequently occur in acromegaly.

Pathologic evidence of extensive left ventricular involvement in arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (also known as arrhythmogenic right ventricular dysplasia) is characterized by adipose or fibroadipose tissue replacement of the right ventricular myocardium, whereas the left ventricle is substantively spared. Two cases of the disease with evidence of extensive left ventricular involvement at pathologic examination are described. Hearts from two patients who died suddenly showed full-thickness right ventricular fatty infiltration associated with extensive left ventricular involvement (> 50% of myocardial thickness). These findings might explain the reported clinical features of left ventricle dysfunction in a subset of patients with arrhythmogenic right ventricular cardiomyopathy. In view of the biventricular involvement of the disease, it should simply be termed “arrhythmogenic cardiomyopathy.”

Left ventricular involvement in right ventricular dysplasia

Right ventricular dysplasia, a heart muscle disease of unknown cause, anatomically characterized by variable replacement of myocardial muscle with adipose or fibroadipose tissue, is usually considered a selective disorder of the right ventricle. However, concomitant left ventricular involvement has been noted in a few cases. The aim of this study was to evaluate the prevalence and characteristics of left ventricular involvement in right ventricular dysplasia, as well as possible progression of the disease. Thirty-nine patients with right ventricular dysplasia were studied by M-mode and two-dimensional echocardiography; 28 of them also underwent cardiac catheterization, and in 25 endomyocardial biopsy was performed. On first examination the left ventricle was normal in 25 patients, whereas in the remaining 14 right ventricular abnormalities were associated with left ventricular involvement, characterized by asynergic areas (12 patients) or diffuse mild hypokinesis (two patients). During follow-up (27 patients, 84.1 ± 66.1 months) 10 patients showed worsening of right ventricular function; in nine the appearance or worsening of left ventricular abnormalities was observed. Five patients died (four in congestive heart failure and one suddenly). Results of postmortem examination (available in two patients) showed atrophy of myocells and a massive fatty and fibrous infiltration of the right ventricular wall, associated with degenerative changes and fibrosis of the left ventricle. In conclusion, right ventricular dysplasia may be associated with left ventricular involvement and the disorder appears to be progressive in some instances.

Left ventricular dysfunction and HLA Bw52 antigen in Takayasu arteritis.

Heart disease is the main cause of death in patients with Takayasu arteritis. It has been reported that this disease is closely related to the presence of HLA Bw52 antigen. To assess the correlation between this antigen and left ventricular involvement, we studied 40 patients with Takayasu arteritis, 21 with and 19 without Bw52, using Tl-201 stress myocardial scintigraphy and echocardiography. Those with Bw52 had a significantly higher incidence of abnormal electrocardiographic findings (67% vs 26%; P < 0.05) and of aortic regurgitation (52% vs 11%; P < 0.05). The echocardiographically determined interventricular septal wall thickness plus left ventricular posterior wall thickness (25 +/- 8 vs 17 +/- 3 mm; P < 0.01) and the left ventricular mass (257 +/- 132 vs 142 +/- 51 g; P < 0.01) were significantly increased in the patients with Bw52. Scintigraphically determined perfusion abnormalities were significantly more frequent in those with Bw52 (76% vs 32%; P < 0.05). These observations indicate that patients with Takayasu arteritis and Bw52 antigen have a more severe left ventricular involvement than the patients without that antigen. The left ventricular impairment may account for the poor prognosis of Takayasu patients with Bw52.

Right Ventricular Infarction

Right ventricular infarction commonly occurs in association with acute inferior left ventricular infarction, but is uncommon when infarction involves other areas of the left ventricle. Evidence of right ventricular infarction often can be detected by physical examination, electrocardiography, echocardiography, or radionuclide ventriculography. However, hemodynamically significant infarction (i.e., hypotension or shock) is much less frequent, occurring in approximately 10% of patients with other evidence of right ventricular infarction. Right ventricular infarction increases ventricular stiffness, thereby impeding diastolic filling. This results in hemodynamic changes similar to those found in constrictive pericarditis: elevated systemic venous pressure, a Y descent greater than the X descent, and an inspiratory increase in venous pressure. The increase in venous pressure generally equals or even exceeds left atrial pressure. When hypotension or shock occurs, expansion of vascular volume is generally employed as initial therapy. In nonresponders, dobutamine or similar inotropic agents may be helpful. The prognosis during the acute phases is guarded, but, in survivors, prognosis is favorable and generally related to the extent of left ventricular involvement.

Left ventricular involvement in right ventricular cardiomyopathy.

The characteristics of left ventricular (LV) involvement in 31 patients with right ventricular cardiomyopathy (RVCMP) were studied by two-dimensional echocardiography (2D echo). Two groups were identified: in group 1 (19 patients) the LV appeared normal initially, but became abnormal in four patients during follow-up. LV involvement was present at diagnosis in the 12 patients of group 2; LV function worsened in one of them. In conclusion, LV involvement is frequent in RVCMP. At least in some cases the disease appears to be progressive.

Left ventricular function during sepsis

The prevalence and prognostic significance of left ventricular involvement in septic patients without shock was investigated. Systolic time intervals (STI) and preejection period/left ventricular ejection time ratio (PEP/LVET) were used to assess left ventricular function. Forty-nine patients, 22 of whom ultimately died, were studied. The group as a whole showed abnormal PEP/LVET ratio (0.40 +/- 0.02) that differed significantly (p less than .01) from reported normal values (0.345 +/- 0.002), demonstrating widespread left ventricular dysfunction in this population. In order to establish the prognostic significance of left ventricular impairment, the population was divided into two groups according to the PEP/LVET ratio. Group 1 (PEP/LVET less than or equal to 0.42) showed a mortality rate of 10/33 (30%), while group 2 (PEP/LVET greater than 0.42) had a significantly greater mortality (12/16 [75%], p less than .001). The test that has a sensitivity of 55%, a specificity of 85%, and a positive predictive value of 75% identifies a subset of septic patients with severe impairment of left ventricular function and high risk of dying.

Relationship between plasma atrial natriuretic peptide and left atrial and left ventricular involvement in essential hypertension.

In order to investigate the role of cardiac hypertrophy in atrial natriuretic peptide (ANP) secretion in patients with essential hypertension, plasma levels of ANP were measured after overnight rest in 36 patients with untreated hypertension and in 31 normotensive controls. In the hypertensive subjects, plasma levels were correlated with left ventricular (LV) and left atrial abnormalities detected by chest X-ray, electrocardiogram (ECG) and M-mode echocardiography. Plasma ANP levels in patients with hypertension averaged 146 +/- 27 pg/ml compared to 46 +/- 7 pg/ml in the normotensive subjects (P less than 0.001). In patients with hypertension a significant correlation was found between ANP and supine systolic blood pressure (r = 0.54, P less than 0.001) and between ANP and diastolic blood pressure (r = 0.38, P less than 0.05). Furthermore, plasma ANP levels were correlated with total heart volume (r = 0.68, P less than 0.01), LV mass (r = 0.525, P less than 0.001), LV posterior wall thickness (r = 0.39, P less than 0.05), Sokolow-Lyon index (r = 0.721, P less than 0.001) and end-diastolic diameter of the left atrium (r = 0.334, P less than 0.05). The results suggest a contribution of LV and left atrial abnormalities to ANP secretion in essential hypertension.

Complex arrhythmias in a patient with predominantly right ventricular cardiomyopathy

A 23-year-old man presented with ventricular tachycardia. The electrocardiogram revealed right bundle branch block plus right axis deviation. It also showed frequent episodes of asystole, 2:1 sinuatrial block and couplets of left bundle branch block morphology. Electrophysiologic study demonstrated sinuatrial entrance block, with an HV interval of 65 msec. It was also possible to induce sustained ventricular tachycardia of left bundle branch block pattern with normal QRS axis. Subsequent investigations were consistent with the diagnosis of right ventricular cardiomyopathy with mild left ventricular involvement.

The efficacy of cibenzoline and propafenone against inducible sustained and nonsustained ventricular tachycardias in conscious dogs with isolated chronic right ventricular infarction: A comparative study with procainamide

The efficacy of intravenous cibenzoline (3 mg/kg), propafenone (4 mg/kg), and procainamide (20 mg/kg) against inducible sustained and nonsustained ventricular tachycardias (VT) was evaluated in 12 consclous dogs with chronic isolated right ventricular (RV) infarction. RV infarct was caused by permanent occlusion of the right coronary artery in the closed-chest dog by intracoronary balloon inflation. Three to 10 days following the occlusion period, programmed electrical stimulation reproducibly induced sustained and/or nonsustained VT, allowing evaluation of antiarrhythmic drug efficacy. Propafenone was effective in preventing the induction of sustained VT in only one out of six dogs tested, but caused a significant ( p < 0.05) slowing of VT rate (269 ± 13 to 230 ± 10 bpm). Procainamide had effects similar to those seen with propafenone. Propafenone and procainamide were ineffective against nonsustained VT, and on established sustained VT once induced. Cibenzoline was effective in preventing the induction of sustained VT in two out of seven dogs, an effect which was not significantly different from either propafenone or procainamide. However, cibenzoline was significantly ( p < 0.05) more effective than either procainamide or propafenone in terminating an established induced sustained VT (four out of six dogs). Furthermore, cibenzoline converted nonsustained to sustained VT in four out of seven dogs tested. Histopathologic studies have shown infarction of the basal two thirds of the RV (38.5 ± 7.8% of the RV) with no left ventricular involvement. It is concluded that the isolated RV infarction model is (1) highly suitable for serial drug testing against inducible VT in consclous dogs, and (2) this model of VT appears to be fairly resistant to standard and newer antiarrhythmic drug therapy.

Inducible sustained ventricular tachycardia and ventricuar fibrillation in conscious dogs with isolated right ventricular infarction: Relation to infarct structure

The susceptibility of infarcted right ventricular myocardium to inducible ventricular tachyarrhythmias was serially evaluated in 18 conscious dogs during the first 2 weeks after permanent right coronary artery occlusion. Properly timed double premature stimuli applied to the right ventricular outflow tract induced sustained (longer than 1 minute) ventricular tachycardia at rates of 190 to 400 beats/min in nine dogs, and ventricular fibrillation in six dogs. No ventricular arrhythmias could be induced in the remaining three dogs. The zone of premature coupling intervals within which ventricular tachyarrhythmias could be induced decreased in each dog as the infarct aged, and by day 12 after occlusion, no ventricular arrhythmias could be induced in any of the dogs studied. Both the size and the degree of patchiness (graded from 0 for no patchiness to +4 for patchiness throughout the infarct) of the infarct appear to be related to the nature of the induced rhythm. Infarcts with greater heterogeneity and those that were larger than 8% of the right ventricular volume were associated with a higher incidence of ventricular fibrillation, and infarcts with a lesser degree of patchiness were more suitable for sustained ventricular tachycardia (3.4 +/- 1.2 versus 1.4 +/- 0.4, p less than 0.05). These findings indicate that the infarcted right ventricular myocardium, independent of left ventricular involvement, can be associated with malignant ventricular tachyarrhythmias, ventricular tachyarrhythmias can be induced only during a well defined postinfarction period; and both the size and geometry of the right ventricular infarct determine the nature of the induced ventricular rhythm.

Right ventricular infarction with shock but without significant left ventricular infarction: A new clinical syndrome

Right ventricular infarction has been described as concurrent with infarction involving the inferior (posterior) aspect of the left ventricular free wall and adjacent interventricular septum. Patients with right ventricular infarction typically show the ECG changes of inferior infarction in leads II, III, and aV F. This report describes two patients with right ventricular infarction but without changes in the QRS complex of the ECG, indicating an inferior infarct of the left ventricle. An autopsy-proven infarct of the right ventricular free wall with neither QRS nor other clinical evidence of left ventricular involvement was responsible for cardiogenic shock and death in one patient. This observation led to a review of a computerized data bank containing records of patients who had undergone cardiac catheterization to determine if there were other patients with clinical criteria suggesting right ventricular infarction without QRS changes of left ventricular infarction. One of the 167 patients with a history of a myocardial infarction also met the following clinical criteria: (1) transiently elevated total creatine kinase and creatine kinase myocardial band; (2) diffuse ST segment elevation without QRS changes indicative of left ventricular infarction on the ECG; (3) normal left ventricular function; (4) hemodynamic evidence of right ventricular dysfunction; and (5) cardiogenic shock.

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = −0.46, p < 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (−1.3 ± 1.8 vs −2.8 ± 1.9 mm, p < 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of −0.2 ± 1.0 vs −1.1 ± 0.5, p < 0.01), whereas in the 15 patients with lateral ST-segment elevation (≥1 mm in lead V 6), precordial ST-segment depression was significantly greater both in absolute terms (−3.5 ± 2.3 vs −1.6 ± 1.7 mm, p < 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of −1.1 ± 0.8 vs −0.5 ± 0.9, p < 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = −0.89, p < 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.