Search

Isolated acute right ventricular (RV) infarction is rare, and ECG diagnosis may be difficult. We report two cases of acute myocardial infarction with ST-segment elevation in anterior precordial leads caused by such an RV involvement. Potential mechanisms for the relationship are given.

To examine the clinical significance of precordial ST-segment changes in patients with acute Q-wave inferior wall myocardial infarction.Prospective evaluation (clinical follow-up) of Q-wave inferior wall myocardial infarction over a 6-year period in patients who fulfilled the inclusion criteria.Coronary care unit at a university hospital.Two hundred consecutive patients with acute Q-wave inferior wall myocardial infarction admitted to the coronary care unit within 24 h from the onset of chest pain.Precordial ST-segment depression resolved24 h (transient) after admission in 84 patients, lastedor = 24 h (persistent) in 48 patients, and was absent in 68 patients, while ST-segment elevation in V4R was detected in 60 patients. Seventy-one patients had major in-hospital complications and 18 patients died in the hospital. When nine variables were used in the multivariate analysis, right ventricular dilatation and persistent precordial ST-segment depression were the important factors related to major in-hospital complications, whereas age, alveolar arterial oxygen difference, and persistent precordial ST-segment depression were important for in-hospital deaths.Left ventricular posterior wall involvement, diagnosed by persistent precordial ST-depression, was an independent and stronger predictor of major in-hospital complications and deaths than right ventricular involvement in patients with acute Q-wave inferior wall myocardial infarction.

Eleven patients with implanted pervenous pacemakers were found to have unusual QRS morphology resembling right bundle branch block (RBBB) on the 12-lead electrocardiogram. In nine patients, the tip of the electrode catheter was established with certainty to be in the right ventricular apex. In eight of the nine, the standard leads showed a left bundle branch block pattern (LBBB), whereas only the precordial leads V 1 and V 2 resembled RBBB. In only one of the nine was the RBBB pattern also seen in the standard leads. In all nine, recording the precordial leads one intercostal space below the usual space eliminated the RBBB pattern in V 1 -V 2 and resulted in inscription of a QS complex, whereas recording the leads one space higher than usual enhanced the height of the R wave. This is explained by the marked superior and slight anterior orientation of the main QRS complex in right ventricular pacing. It is suggested that the pattern of RBBB in V 1 -V 2 +LBBB in lead 1 be named pseudo RBBB pattern since it does not represent left prior to right ventricular activation.

T-wave polarity in V1 to V3 was examined in 70 patients with acute inferior wall myocardial infarctions (IWMI) as an indicator of significant disease in the left anterior descending coronary artery (LAD). Fifty-three percent (37/70) had precordial T-wave inversions, and of these 38 percent (14/37) had angiographically significant LAD disease. Conversely, 47 percent (33/70) had upright T waves in V1 to V3, and of these, 52 percent (17/33) had significant LAD disease. Likewise, 41 percent of the patients with ST segment depression in V1 to V3 had significant LAD disease, while 50 percent of those with isoelectric ST segments were similarly affected. Finally, only 39 percent of those patients with both precordial ST segment depression and T-wave inversion had significant LAD disease. We conclude that neither anterior ST depression, T-wave inversion, nor a combination of both is a sensitive or specific indicator of LAD disease in patients with acute IWMI.

The effects of intravenous therapy with propranolol (0.15 mg/kg of body weight) on changes in hemodynamics and the sum of precordial elevations of the S-T segment (∑ST) were studied 8.5 hours after the onset of pain in 14 patients with acute anterior transmural myocardial infarction and without complication. Therapy with propranolol (7.5 to 15 mg) produced a significant and sustained decrease from control in ∑ST, amounting to 46 percent (from 41 to 22 mm; P

An unusual, high-pitched, early diastolic sound coinciding with a prominent, sharp precordial pulse was observed in a patient with a large chronic pericardial effusion. The pulse and sound coincided exactly with the anterior excursion of the heart within the fluid-filled pericardial sac, suggesting that the sound and pulse result from the ballistic effect of the heart striking the anterior pericardium and chest wall. This finding may be specific for large pericardial effusion with a "swinging heart."

Tall precordial T waves can be found in a proportion of normal Indian subjects (2.5 percent). A significantly higher incidence (10.4 percent) was found in those with ischemic heart disease. In younger subjects the chance of tall T waves as a normal finding is high, whereas in persons 40 years of age or older it is more likely a pathologic condition. Women had a strikingly lower incidence of such T waves, in that none of the normal female subjects exhibited a tall T wave. Determination of the QRS axis and ventricular gradient are suggested as means of differentiating pathologic tall T waves from tall T waves in normal subjects.

A 64-year-old woman with an acute exacerbation of chronic relapsing pericarditis had initial clinical and ECG features that were consistent with an acute anterior myocardial infarction. Transient Q waves were observed in the precordial leads, and she also exhibited elevated plasma MB creatine kinase (MB CK) activity. However, the overall clinical and laboratory data, including angiographic and radionuclide studies, suggest that the myocardial damage was secondary to pericarditis per se, rather than ischemic myocardial infarction. This case emphasizes that Q waves and elevated MB CK activity can be seen in association with pericarditis, and this must be differentiated from myocardial infarction secondary to coronary artery disease.

A patient had repetitive ventricular fibrillation preceded by alternating ST segment depression and elevation. The ECG changes were confined to the precordial leads only, reflecting subendocardial and transmural ischemia, respectively. It is speculated that the patient exhibited consecutive episodes of subtotal and total coronary occlusion, both episodes being critical enough to induce lethal arrhythmias.

A patient with anterior myocardial infarction had bilateral pneumothoraces. Left pneumothorax was associated with reappearance of precordial R waves, while right pneumothorax caused no ECG change. This previously undescribed finding suggests the importance of air insulating the chest wall, rather than cardiac rotation, dilatation, or displacement as a mechanism of the ECG change.

In 68 patients, subxiphoidal, percordial, and suprasternal echocardiography was used to trace the Swan-Ganz catheter during its passage to the pulmonary artery and to localize its position. The localization of the catheter could be exactly identified in 62 out of 68 patients in whom we managed to obtain a suprasternal echocardiogram. In one patient, the catheter was found (by chest x-ray film) in the left pulmonary artery (LPA) and was regarded to be in the right pulmonary artery according to suprasternal echocardiography. In two patients, the catheter could not be localized by suprasternal echocardiography although it was positioned in the LPA. In three patients, the catheters could not be advanced to the pulmonary circulation and were visualized within the right ventricular cavity by precordial and subxihpoid echocardiogarphy. Thus, echocardiography, particularly the suprasternal approach, has proven a safe, reliable, and easy way for position control of Swan-Ganz catheters.

T all T waves in the precordial leads may manifest in many and varied conditions. Hyperkalemia is one of the most common. This presentation reflects two cases of severe hypokalemia which manifested with unusually tall and peaked precordial U waves. The presentation in one of the cases closely simulated the tall T-waves of hyperkalemia.

A patient with rheumatic mitral valve stenosis and regurgitation presented with shortness of breath and a "noise" in her chest. Cardiac auscultation revealed an intermittent late systolic "whoop." An increase in severity of mitral valve insufficiency during the periods of "whoop" was observed by pulsed Doppler, hemodynamic tracings and left ventriculography.

An unusual case of arteriovenous communication between the left inferior epigastric artery, a branch of the femoral artery, and the superior vena cava is presented. The communication caused a continuous murmur at the lower parasternal area and was responsible for a significant left-to-right shunt. Surgical treatment, which consisted of ligation of the aberrant artery at its origin, was followed by disappearance of the precordial murmur.

The usefulness of the electrocardiographic sign of "low voltage" in the diagnosis of pericardial effusion was investigated in 122 patients comprising three study groups. Sixty-four patients (group 1) had a pericardial effusion detected and measured by echocardiographic studies. The volume of the effusion showed no correlation with electrocardiographic voltage. A second group of 36 patients was identified as having low voltage on routine electrocardiograms. Only 13 (36 percent) had echocardiographically demonstrable pericardial effusion. Group 3 consisted of 22 patients who required pericardiocentesis. The ECGs obtained immediately after pericardiocentesis showed an increase in average voltage of 0.48 mm in the limb leads and 0.83 mm in the precordial leads for each 100 ml of fluid removed. This study demonstrates that a single ECG with "low voltage" is not useful in the diagnosis of pericardial effusion but that a reduction in the voltage of serial ECGs may suggest the development of pericardial effusion.

The incidence and duration of right precordial electrocardiographic signs of early right ventricular enlargement were investigated in cases of acute pulmonary embolism. These signs consist of slurring of the ascending limb of the “S” wave in the right precordial leads and regression of the R/S ratio between two successive precordial leads. These changes were observed in 74 of 127 tracings taken at or soon after the onset of symptoms. A correlation was demonstrated between right precordial patterns associated with progressive right ventricular enlargement and the extent of pulmonary arterial occlusion as determined by autopsy or surgery. The electrocardiographic signs under investigation were found to occur more frequently in acute tracings than other patterns associated with acute pulmonary embolism. The presence of right precordial signs of early right ventricular enlargement in acute and serial tracings taken at short intervals provide assistance in the diagnosis, as well as in determining the management of acute pulmonary embolism.

Pneumomediastinum and subcutaneous emphysema are unusual complications of acute bronchial asthma. The diagnosis may be suspected by the onset of precordial chest pain, a “crunching” precordial systole sound and may be confirmed by the roentgenographic evidence of air in the mediastinum. Treatment should include 100 percent oxygen atmosphere and careful treatment of the underlying asthma.