Inferior myocardial infarction with extension to the right ventricle due to a huge clot in the ascending aorta that invaded the right coronary artery - A case report

Influence of Second- and Third-Degree Heart Block on 30-Day Outcome Following Acute Myocardial Infarction in the Drug-Eluting Stent Era

Inferior ST-segment myocardial infarction (STEMI) is often due to acute occlusion of the right coronary artery (RCA) or left circumflex artery (LCx). Anatomically, distal occlusion of a dominant left anterior descending artery (LAD) wrapping around the apex supplying posterior descending artery (PDA) can also lead to inferior wall MI. The occurrence of inferior MI with LAD occlusion is underappreciated. We are presenting a case of proximal LAD occlusion leading to inferior wall MI in the presence of non-occlusive right coronary artery (RCA). Physicians should keep in mind the possibility of inferior myocardial infarction with LAD occlusion and interventional cardiologists should perform a complete angiogram to identify the faulty lesion in inferior STEMI before deciding on a RCA or LCx as the culprit artery. Isolated IWMI (inferior wall myocardial infarction) from proximal occlusion of the wrapped around LAD as noted in our patient is a rare occurrence.

This study was performed to assess the accuracy of standard electrocardiographic criteria in diagnosing of right ventricular (RV) involvement in patients with inferior myocardial infarction (IMI). This was a retrospective analysis of patients admitted with an IMI. Proximal occlusion of the right coronary artery before the origin of the RV branch on angiography was considered diagnostic of RV involvement. The subjects were 129 patients (mean age = 55.8±13.1 years; 81.4% male) with inferior ST-elevation myocardial infarction. The most sensitive indicators of RV involvement were an ST elevation in V4R (72.9%) and a higher ST elevation in lead III than in lead II (80.4%). The most specific indicators were ST elevation in V1 (88.7%) and ST elevation in V1 with ST depression in V2 (97.1%). Combining all the criteria improved sensitivity to 85.7% but reduced specificity to 21.2%. No single electrocardiogram criterion was able to identify all cases of RV involvement in patients with IMI. Combining the different criteria helped pick up more cases at the cost of increasing false positives.

49-Year-Old Woman With Chest Pain

The use of cocaine has evolved from chewing the leaves of the Erythroxylon coca bush thousands of years ago, to purification of cocaine hydrochloride over 100 years ago and its use in tonics and elixirs (at one time in popular cola drinks), to insufflating and injecting the fine, white, water-soluble, powder form, to a smokable freebase form called “crack,” which became popular in the 1980s.1 In 2007, 2.1 million Americans had recent cocaine use; 1.6 million met criteria for cocaine dependence or abuse.1 Cocaine accounted for 31% of all visits to the emergency department related to drug misuse or abuse.1 From 1971 to 1987, the incidence of deaths caused by cocaine overdose increased 20-fold in Dade County, Florida.2 In a consecutive series of 233 emergency visits by cocaine-using patients, 56% presented with cardiovascular complaints, including 40% with chest pain.3 A minority of these patients have acute myocardial infarction (MI) (≈6%),4,–,7 and overall mortality is low (<1%).3,–,5,8,–,10 However, cocaine is associated with a number of cardiovascular diseases, including MI, heart failure, cardiomyopathies, arrhythmias, aortic dissection, and endocarditis. Identifying patients with acute disease is challenging. This review describes the relationship between cocaine and various cardiovascular diseases, as well as appropriate diagnostic evaluation and therapies. ### Molecular Cocaine stimulates the sympathetic nervous system by inhibiting catecholamine reuptake at sympathetic nerve terminals,11,12 stimulating central sympathetic outflow,11 and increasing the sensitivity of adrenergic nerve endings to norepinephrine (Figure 1).12 Cocaine also acts like a class I antiarrhythmic agent (local anesthetic) by blocking sodium and potassium channels, which depresses cardiovascular parameters.13 Of these 2 primary, opposing actions, enhanced sympathetic activity predominates at low cocaine doses, whereas the local anesthetic actions …

Acute myocardial infarction (MI) involving only the right ventricle is an uncommon event. Right ventricular myocardial infarction has been an independent predictor of major complications and mortality. Electrocardiogram (ECG) through right precordial leads (V4R) is a useful & convenient tool of diagnosing right ventricular infarction. Standard surface ECG by using V4R could aid clinical recognition of concomitant right ventricular infarction in patients with inferior wall myocardial infarction. Increasing age, male sex & previous history of ischemic heart disease were found to be important risk factors for the occurrence of right ventricular infarction. Keyword: electrocardiography, inferior wall myocardial infarction, myocardial infarction, right ventricular function. Myocardial performance index, Tricuspid annular motion I. Introduction Inferior wall of the heart is formed by both left ventricle and right ventricle. In about 50 percent of the patient with inferior wall myocardial infarction (1, 2, 3), the right ventricle is involved. Recognition of right ventricle infarction is important because of its various hemodynamic consequences. Presence of right ventricular myocardial infarction may enforce an increased risk of shock, arrhythmia and death in inferior wall myocardial infarction (4). The increased risk is related to the presence of right ventricle involvement itself rather than the extent of left ventricular myocardial damage (5). Inferior wall myocardial infarction patients with right ventricular infarction comprises a high risk subset of patient with a mortality rate as high as 25 to 30 % as opposed to an overall mortality rate of approx 6 % of patients with inferior myocardial infarction without right ventricular infarction. Occlusion of proximal dominant RCA is usually responsible for right ventricular infarction in inferior wall myocardial infarction (6). Right ventricular function has not widely been studied after a MI unlike a LV function. There is right ventricular involvement in more than 1/3 rd of patients with acute inferior wall myocardial infarction. Right ventricle involvement has been reported to be an independent predictor of major complications and in hospital mortality after acute MI (7). ST segment elevation in right precordial lead, V4R is one of the most reliable echocardiographic signs of acute right ventricular infarction. ECG is one of the major diagnostic tool being cost effective and easily available. A hypokinetic or akinetic segment of RV observed by ECG can also be used to detect RV dysfunction after right ventricular infarction. The presence of ST segment elevation on leads II, III, and AVF on ECG are always suggestive of RVI (8, 9). The present study has been made to estimate the correlation using clinical examination and surface ECG.

Incidental Finding of a Coronary Artery Fistula in a Patient With Anterolateral ST-Elevation Myocardial Infarction

ST elevation measurements differ in patients with inferior myocardial infarction and right ventricular infarction

Background. Left ventricular (LV) remodeling is greater in patients with anterior myocardial infarction (MI) compared to those with inferior MI. Left atrial (LA) remodeling is expected to have influences from both LV remodeling and mitral valve dysfunction or mitral regurgitation (MR), which is more frequent in inferior MI. Therefore, LA remodeling may not necessarily be less in inferior MI compared to anterior MI. The purpose of the study is comparison of LV and LA remodeling in patients with anteroseptal and inferior MI with or without MR.Methods. In 61 consecutive patients with prior anterior MI, 33 with prior inferior MI, and 22 normal control subjects, LV and LA volumes were measured using biplane Simpson's method, and MR fraction was quantified by Doppler echocardiography.Results. Although patients with inferior MI had significantly less LV dilatation (LV end-diastolic volume: 91±11 vs. 125±45 vs. 106±19 ml, control vs. anterior vs. inferior, p 20%) was significantly higher in patients with inferior MI compared to anterior MI (7/61 vs. 12/33, p<0.01). In selected patients without significant ischemic MR, LA dilatation was comparable between inferior and anterior MI (60±28 vs. 61±16 ml, n.s.).Conclusions. Compared to patients with anterior MI, LV remodeling is significantly less but LA remodeling is significantly greater in inferior MI, suggesting the important role of ischemic MR to induce LA remodeling.

Wolff-Parkinson-White Syndrome Simulating Inferior Myocardial Infarction in a Cocaine Abuser for Urgent Dilation and Evacuation of the Uterus

We appreciated reading the paper by Ibrahim et al. [1] describing the impact of K2 abuse on sudden cardiac death (SCD). This paper, although it provides interesting information about synthetic cannabinoid (SC), it also presents several limitations. Notably, the authors formally connected the K2 abuse and the SCD. In contrast to Ibrahim et al., we think that the SCD is mainly related to the cardiac history of the patient. Substantial evidence supports our point of view. First, the patient had a past cardiological history with a previous myocardial infarction (MI) and four-vessel coronary artery bypass graft 10 years ago. Authors did not specify where the MI was located but we can suppose, from the electrocardiogram (ECG) in sinus rhythm, that it was an inferior MI (Q wave in inferior derivations). Moreover, authors did not specify the exact coronary lesions in native vessels. It would be interesting to know if one vessel (right coronary artery) was occluded. All these elements are important because it is well established that most of SCD cases in coronary artery disease patients occur on previous myocardial scar (which is the consequence of a coronary artery occlusion and results in the presence of Q wave in a coronary artery territory) and typically 10 years after MI [2–4]. Another element that supports our hypothesis is that authors declare that “the cardiac arrest was not associated with an acute coronary occlusion” [1] which is largely in favor of our theory. So it seems more reasonable to think that cardiac arrest is the consequence of a malignant reentrant ventricular arrhythmia than K2 abuse [2, 3]. It seems also difficult to conclude a myocardial necrosis based on moderate troponin T elevation (0.632). It would be helpful to specify the laboratory standards for the troponin T. The moderate elevation seems more likely due to the resuscitation (drugs, defibrillation, cardiac massage…) than a real myocardial necrosis which usually leads to major troponin T elevations [5]. Second, we have serious concerns regarding some cardiological interpretation of this observation. In fact, authors interpreted the ECG on admission [1] as a sinus tachycardia. It is wrong. This ECG shows a typical atrial flutter with a 2/1 ventricular conduction. We can recognize the atrial flutter with a regular and typical atrial activation near 240/min, uniform and continuous in all leads, with the typical “sawtooth” pattern in the inferior leads (manifested by a notching of the end of the QRS complex, clearly visible in V1 derivation and disappears during sinus rhythm in the second ECG presented by Ibrahim et al.). There is a classically 2 : 1 ventricular response [6]. The very long PR interval observed during tachycardia and absent in sinus rhythm also indicated that the rhythm cannot be sinusal in the first ECG. Atrial flutter following a cardiac arrest is classical when using drugs such as epinephrine or adrenaline and disappears most frequently in few hours or a day [7]. Regarding ECGs, we agree that cannabinoids have an impact on several ion channels but it seems difficult to directly link these properties to ECG changes, especially since the patient already has changes on his baseline ECG due to his coronary artery disease (and possibly antiarrhythmic drugs). Third, evidence supports that cannabis is now a well-known trigger for MI [8, 9]. However, the challenge remains to link clearly the cardiac event to cannabinoids consumption and case reports are most often published without a clear etiology, with conclusions which are therefore most speculative. Conversely, the SC impact on serious cardiac events remains to date unknown, even if there are serious concerns [10–15]. The increasing use of SC as drug of abuse and their consequences in terms of public health have, therefore, to be closely monitored, especially considering pharmacological properties as the higher affinity for cannabinoid receptors than natural cannabinoid delta-9 THC resulting in higher pharmacological activity, early demonstrated with first SC [16, 17]. This present case report by Ibrahim et al. is therefore consistent with previously published reports but, to our knowledge, cannot reliably connect SC and SCD. In conclusion, there are several evidences [10–15] to think that cannabis and SC can lead to serious cardiac disorders but we think that this case report is speculative rather than affirmative (because of the study limitations described above) and therefore, conclusions should be more modulated.

Resolution of ST-segment elevation is the best bedside predictor of myocardial reperfusion. This study was conducted to examine the resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior acute myocardial infarction (MI) and to corroborate it with echocardiographic and coronary angiographic data. The study population consisted of 70 patients, 35 each in the anterior and inferior MI groups. The electrocardiograms (ECGs) were recorded before, on completion of, and on Days 1 and 2 post streptokinase therapy. The resolution of ST segment determined from post-streptokinase ECGs was compared between the two groups and correlated with echocardiographic and coronary angiographic data. On completion of and on Day 1 post streptokinase therapy, ST-segment resolution in both groups was not significantly different. On Day 2 post streptokinase therapy, resolution of the ST segment per lead was significantly lower in anterior than that in inferior MI (61 +/- 21% anterior vs. 77 +/- 21% inferior, p 0.003). The number of patients with akinesis of infarct-related ventricular wall was significantly higher (17 anterior vs. 7 inferior, p 0.02), and left ventricular ejection fraction was significantly lower in anterior MI (39 +/- 7% anterior vs. 48 +/- 8% inferior, p < 0.01). There was no significant difference in coronary angiographic data. One patient in each group demonstrated normal coronary arteries. The resolution of ST-segment elevation on the completion of and on Day 1 post streptokinase therapy was comparable between anterior and inferior MI. The significantly less frequent resolution of ST-segment elevation in anterior MI on Day 2 post streptokinase could be due to more akinesis, larger infarct size, and worse systolic function rather than due to failure to open the infarct-related vessel.

Influence of right bundle branch block on short- and long-term survival after inferior wall Q-wave myocardial infarction

Right and left circumflex coronary artery occlusions cause inferior myocardial infarction. Coronary artery dominance influences the amount and anatomic location of myocardium that is perfused. In patients with acute inferior ST- elevated myocardial infarction (STEMI) the impact ot coronary dominance on atherosclerosis progression is unknown. Our study evaluated the association between coronary dominance and STEMI related artery.

New surgical strategies to restore the saddle shape of the mitral annulus are expected to increase annuloplasty effectiveness. Preoperative and postoperative configuration of the curved annulus, however, is difficult to quantify with 2-dimensional echocardiography. We sought to investigate the geometric deformity in the mitral annulus in ischemic mitral regurgitation (MR), comparing inferior and anterior myocardial infarction (MI) with the use of a custom quantitation software system with transthoracic 3-dimensional echocardiography. We performed real-time 3-dimensional echocardiography in 23 patients with ischemic MR attributable to inferior MI or anterior MI and in 10 controls. Three-dimensional data were cropped into 18 radial planes, and we manually marked the annulus in mid systole. Three-dimensional annular images were reconstructed, and annular circumferences, areas, and heights were quantified. Annulus was significantly more dilated and flattened in ischemic MR than in controls and was further deformed in anterior MI as compared with inferior MI (control: circumference 9.9+/-0.7 cm, area 9.6+/-0.5 cm2, height 5.0+/-0.7 mm; inferior MI: circumference 11.5+/-1.2 cm [P<0.01 compared with control], area 11.4+/-2.0 cm2 [P<0.05 compared with control], height 3.5+/-1.6 mm [P<0.05 compared with control]; anterior MI: circumference 14.2+/-2.4 cm [P<0.0001 compared with control, P<0.05 compared with inferior MI], area 13.7+/-2.8 cm2 [P<0.01 compared with control, P<0.05 compared with inferior MI], height 1.7+/-1.5 mm [P<0.0001 compared with control, P<0.05 compared with inferior MI]). Mitral annulus flattens in ischemic MR. Deformity of the mitral annulus was greater in anterior MI group than in the inferior MI group.