Inferoseptal myocardial infarction: Another cause of precordial ST-segment depression in transmural inferior wall myocardial infarction?

Electrocardiographic ST-segment depression in the anterior precordial leads is a frequent observation during the initial hospital phase of acute transmural inferior myocardial infarction (MI), but is of uncertain significance. No available clinical studies have examined the prevalence of inferoseptal necrosis complicating inferior MI. Therefore, the clinical course, electrocardiographic features, radionuclide angiograms and cardiac enzyme changes in 57 patients with transmural inferior MI who did not have prior anterior or concomitant "true posterior" MI, associated anterior or posterolateral asynergy by radionuclide ventriculography, or left or right bundle branch block were reviewed retrospectively. Patients were categorized according to the presence (group A) or absence (group B) of precordial ST-segment depression and according to the presence (group I) or absence (group II) of radionuclide septal wall motion abnormalities. There were no significant differences in global left ventricular ejection fraction (group A, 49 +/- 8, group B, 52 +/- 41; group I, 51 +/- 7, group II, 51 +/- 6), right ventricular ejection fraction (group A, 45 +/- 9, group B, 42 +/- 7; group I, 43 +/- 8, group II, 41 +/- 8), or clinical outcome in the hospital. However, chi-square analysis revealed a significant (p less than 0.05) association between the presence or absence of septal asynergy and the presence or absence of precordial ST depression. In addition, average peak creatine kinase elevation (group I, 761 +/- 164 IU; group II, 698 +/- 178 IU) attained marginal significance by paired t test (p = 0.06). Precordial ST-segment depression during transmural inferior MI is frequently associated with septal asynergy by gated radionuclide angiography (15 of 26 patients, 58%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute myocardial infarction: what is new?

Current recommendations on the management of acute myocardial infarction and the use of thrombolysis are reviewed.     

Could missile attacks trigger acute myocardial infarction?

OBJECTIVE: During the Gulf war in 2003, Kuwait was targeted with missile attacks for 10 consecutive days. Our objective is to evaluate the influence of missile attacks on the incidence of acute myocardial infarction (AMI). METHODS AND RESULTS: We retrospectively compared the number of admissions for AMI presenting to a major general hospital during missile attacks period (MAP) in 2003 with four control periods. MAP and each control period consisted of the same number of days (10 days). The four control periods were the 10 days immediately before and after MAP; and the same time period as MAP for the years 2001 and 2002.The number of admissions for AMI was highest during MAP, 21 cases compared to 14-16 cases in the four control periods, with a trend towards increase during MAP (incidence rate ratio = 1.59; 95% CI 0.95 to 2.66, p < 0.07). The number of admissions for AMI during the first 5 days of MAP was significantly higher compared to the first 5 days of the four control periods (incidence rate ratio = 2.43; 95% CI 1.23 to 4.26, p < 0.01). The observed AMI admission rate during the first 5 days of MAP was significantly higher than expected for a 5-day period in the years 2001, 2002 and 2003. This increase was specific to AMI and did not affect other acute cardiac conditions. CONCLUSIONS: Missile attacks were associated with an increase in the incidence of AMI. This increase was specific to AMI and did not influence acute cardiac conditions.     

Is anteroseptal myocardial infarction an appropriate term?

Anteroseptal myocardial infarction is defined by the presence of electrocardiographic Q-waves limited to precordial leads V(1) to V(2), V(3), or V(4). We sought to determine whether this term is appropriate by correlating electrocardiographic, echocardiographic, and angiographic findings.We studied 50 consecutive patients admitted for a first acute myocardial infarction with Q-waves in precordial leads V(1) to V(2)-V(4), and who had undergone echocardiography and coronary angiography during hospitalization. Echocardiograms in the apical long-axis, two-chamber, and four-chamber views were studied using a wall motion scoring index.Q-waves were present in precordial leads V(1)-V(2) in 4 patients, V(1)-V(3) in 28 patients, and V(1)-V(4) in the remaining 18 patients. The presumptive culprit lesion was in the proximal segment of the left anterior descending artery in 15 patients, in the middle segment in 33 patients, and indeterminate in 2 patients. This lesion was before the first septal branch in 19 patients and after the first septal branch in 29. Mean (+/- SD) left ventricular ejection fraction was 51% +/- 10%. Echocardiographic analysis showed that the septal wall was never the only wall that was affected. However, the apex was affected in all patients and was the only wall that was affected in 26 (52%) patients (apical wall index, 2.1 +/- 0.5). In the remaining 24 patients, the septum was also affected (septal index, 1.5 +/- 0.3), but less severely than was the apex (apical index, 2.3 +/- 0.4; P <0.0001 vs. septum). In these 24 patients, the anterior and lateral walls were also affected (anterior index, 1.4 +/- 0.4; lateral index, 1.1 +/- 0.2), but again, less severely than was the apex (P <0.0001 for both vs. apex).Neither angiographic nor echocardiographic data support the notion of an isolated anteroseptal myocardial infarction. Left anterior descending artery involvement appears more often to be midsegment and postseptal. The apex is always and principally affected. These findings suggest that anteroseptal myocardial infarction is a misnomer and that the V(1) to V(2)-V(4) Q-wave pattern should be considered to indicate a predominantly apical, and generally limited, myocardial infarction.     

Ischemia-reperfusion induces myocardial infarction through mitochondrial Ca²⁺ overload

Both mitochondria and the sarcoplasmic reticulum (SR) are essential for myocardial homeostasis and control of cardiac function. Uptake of Ca(2+) from the cytosol into SR is mediated by the Ca(2+)-dependent ATPase SERCA2a, which is reversibly inhibited by phospholamban (PLN). We previously showed that removal of PLN inhibition of SERCA2a with an antibody to (anti-) PLN reduces cytosolic Ca(2+) overload, thereby attenuating the spread of contraction bands and fodrin proteolysis, during reperfusion after cardiac ischemia. We have now examined the effects of anti-PLN injection into the heart on the development of myocardial infarction (MI) after ischemia-reperfusion in rats. Whereas anti-PLN injection attenuated cytosolic Ca(2+) overload, it did not affect MI size 6h after the onset of reperfusion and actually increased it at 30 min. The antibody also increased the release of apoptosis-inducing factor (AIF) from mitochondria into the cytosol, indicative of enhanced opening of the mitochondrial permeability transition pore (mPTP). Administration of an mPTP blocker at the time of reperfusion or of a blocker of the mitochondrial Ca(2+) uniporter significantly suppressed the release of AIF and the development of MI. These results indicate that the enhancement of SR Ca(2+) loading by anti-PLN injection facilitated Ca(2+) uniporter-dependent mitochondrial Ca(2+) uptake and thereby induced mPTP opening and MI development during early reperfusion. The enhancement of SR Ca(2+) loading thus aggravates MI in a manner independent of cytosolic Ca(2+) overload. Given that cytosolic Ca(2+) overload induces contraction bands, our findings are inconsistent with a causal relation between contraction bands and MI.