Diaphragmatic Myocardial Infarction Research Articles

PDA (Posterior Descending Artery) & Coronary Dominance-A MDCT Coronary Angiographic Analysis of Anatomic Variations and Clinical Importance

Introduction: There is considerable variation in the arterial supply of diaphragmatic surface of the heart. Diaphragmatic myocardial infarction is one of the more common consequences of coronary artery disease. The aim of this study was to assess the incidence of anatomic variants of origin and termination of Posterior Descending Artery (PDA) and to determine the type of coronary dominance in North Indian population. Subjects and Methods: This prospective study was carried out on 50 routine subjects of different age groups who came to the Department of Radiodiagnosis, King George’s Medical University UP, Lucknow in the year 2010- 2011 with known or suspected coronary artery disease. All the cases were investigated on a 64 slice Multidetector Computed Tomographic (MDCT) scanner, using retrospective Electrocardiographic gating. Endeavour was made to determine the incidence of sites of origin and termination of PDA as well as to determine the type of coronary dominance. Results: PDA arose from Right Coronary Artery (RCA) in 39 (78%) cases and from Left Circumflex (LCx) artery in 11(22%) cases. The PDA was found to terminate in the upper 1/4 of Posterior Inter-Ventricular Groove (PIVG) in 18 (36%) cases, in upper 1/2 of PIVG in 19 (38%) cases, in upper 3/4 of PIVG in 10 (20%) cases and at the apex of the heart in 1 (2%) case. None of the female had termination of PDA at the apex. Termination of PDA could not be determined in 2 (4%) cases. Right dominance was seen in 36 (72%) cases, Left dominance in 11 (22%) cases. and Co-dominance in 3 (6%) cases. Conclusion: Posterior descending artery most commonly terminated after traversing the upper half of posterior inter-ventricular groove. The incidence of left coronary dominance was more in females, it was approximately twice the incidence found in males. Co-dominance was observed only in male subjects.

Evaluation of exercise-induced Q-wave amplitude changes and their clinical value

We studied the influence of exercise level, severity of coronary artery disease (CAD), presence of previous myocardial infarction (MI), anterior or diaphragmatic, on the clinical value of exertional Q wave changes (Delta-Q). We retrospectively evaluated the exercise electrocardiograms of 62 patients without angiographic evidence of CAD and 133 patients with CAD; 28 of them had single (SVD) and 105 multivessel disease (MVD). Forty-one patients had a previous diaphragmatic MI and 23 anterior. The sensitivity, specificity and predictive value of Delta-Q were compared to the ST criterion. The exercise level affected Delta-Q. ST and Delta-Q had similar specificity and predictive values. The extent of CAD did not affect the sensitivity of Delta-Q and this method was better than ST to detect SVD patients. The Delta-Q criterion was equally as efficient as ST in MVD patients without MI and with diaphragmatic MI. The loss of septal forces on resting electrocardiograms made useless Delta-Q analysis on patients with anterior MI. The improvement of sensitivity in SVD patients by Delta-Q might be of clinical value since these latter are frequently not diagnosed by the ST criterion.

Extracardiac left to right shunt in a patient with biventricular postinfarction rupture and pseudoaneurysm

A 68 year old man had a diaphragmatic myocardial infarction and 9 months later was admitted with severe congestive heart failure (functional class IV). Cardiac catheterization demonstrated a postinfarction pseudoaneurysm. Because of a massive left to right shunt (pulmonary to systemic flow ratio = 2.7), concomitant rupture of the ventricular septum was suspected. At surgery the pseudoaneurysm communicated with the right ventricle through two different orifices and with the left ventricle through another ostium. The ventricular septum was intact. Therefore, the shunt was extracardiac through the pseudoaneurysm (left ventricle----pseudoaneurysm----right ventricle). The unique combination of lesions allowed the patient to survive. The false aneurysm was excised and primary repair was performed in the orifices of the right and left ventricular walls. The postoperative course was uneventful and 10 months later the patient was in functional class I.

The giant R wave of acute myocardial infarction.

The common clinical electrocardiographic criteria for diagnosis of acute transmural myocardial infarction include ST segment elevation and tall, upright T waves, but do not include changes in QRS morphology. The purpose of this study was to show that development of a 50% or greater increase in R wave amplitude, the giant R wave, in patients with acute transmural myocardial infarction occurs, and also to characterize changes in QRS morphology which may aid the ECG diagnosis of acute transmural myocardial infarction. Over the past 6 years, 36 patients with an increase in R wave amplitude during acute transmural myocardial infarction were identified at the Strong Memorial Hospital Coronary Care Unit. A significant increase in R wave height (0.33 +/- 0.10 to 0.97 +/- 0.08 mV, p less than 0.05), width (0.03 +/- 0.00 to 0.08 +/- 0.01, p less than 0.05) and area (0.01 +/- 0.00 to 0.05 +/- 0.01 mV-msec, p less than 0.05) appeared in the same ECG lead demonstrating ST segment elevation and tall T waves during the acute phase of transmural myocardial infarction. Patients with diaphragmatic myocardial infarction showed a significant (p less than 0.05) rightward QRS frontal plane axis shift and patients with anterior wall myocardial infarctions developed an anterior QRS axis shift in the horizontal plane during occurrence of the giant R wave. We conclude from this preliminary study that the giant R wave may be observed during acute transmural myocardial infarction and may in part be caused by local intramyocardial conduction delay in acutely ischemic tissue as supported by an increase in the R wave width along with shifts in the frontal and horizontal plane QRS axis toward the area of acute ischemia. The giant R wave occurs in conjunction with ST segment elevation and tall T waves and may aid the ECG diagnosis of acute transmural myocardial infarction.

Protective role of collaterals in patients with coronary artery occlusion

We reviewed the clinical, hemodynamic and angiographic data of 105 patients with right coronary artery occlusion and of 82 patients with left anterior descending coronary artery occlusion, subdivided into 3 groups by the presence and quality of collaterals to the occluded coronary (absent, poor or good collaterals). We found that patients with right coronary artery occlusion and good collaterals had a lower frequency of diaphragmatic myocardial infarction (60%) than patients with absent collaterals (100%) ( P < 0.01). In addition, in patients with old diaphragmatic myocardial infarction, both poor and good collaterals were associated with a lower frequency of severe asynergy of the diaphragmatic left ventricular segments at left ventriculography (54% and 14%, respectively), compared to patients with no collaterals to the right coronary artery (92%, P < 0.02 vs. poor collaterals, P < 0.001 vs. good collaterals). In contrast, in patients with left anterior descending coronary artery occlusion, the presence of either poor or good collaterals to the left anterior descending coronary artery was not associated with a lower frequency of old anterior myocardial infarction, or, in patients with old anterior myocardial infarction, with a less severe asynergy of the anterior left ventricular segments. Our results suggest that collaterals are effective in protecting the diaphragmatic left ventricular wall in patients with right coronary artery occlusion, but not the anterior left ventricular wall in patients with left anterior descending coronary artery occlusion.

True Posterior Myocardial Infarction

Although the standard 12-lead ECG is useful in establishing the diagnosis of myocardial infarction, its value is limited in determining the exact anatomic location and the extent of the infarction.^1,2 The ECG terminology of infarct location with use of a host of terms like "anterior," "septal," "high lateral," "lateral," "inferior," "posterior," "diaphragmatic," "apical," "basal," "true posterior," "anterobasal," "anteroseptal," "inferolateral," and so forth implies a capability for spatial resolution. However, there is evidence that the ECG provides inadequate information for such a detailed and exact classification.^1'3Thus, these terms often describe ECG distinctions rather than precise anatomic distinctions. The term "posterior infarction" in the older ECG literature was used to denote what is now called "inferior or diaphragmatic myocardial infarction." The term<i>true posterior infarction</i>(also known as "high posterior," "strictly posterior," "pure posterior," "posterobasal, inferobasal, or dorsal paravertebral") refers to involvement of the posterior aspect or infra-atrial part

Lidocaine and Sinus Standstill-Reply

In Reply.— We consider the therapeutic dose of lidocaine when the drug is given at a dosage of no more than 1 to 2 mg/kg of body weight as bolus and no more than 55 μg/kg/min as maintenance drip infusion. If heart failure and liver disease are present, the dosage must be reduced. In the case reported by Cheng and Wadhwa (1973;223:790), the patient received 200 mg of lidocaine over five minutes and had severe congestive heart failure; we think that the dose, as previously pointed out by Cacace (1973;224:1428), was excessive and that sinus standstill after lidocaine administration, together with hypotension and convulsions, was the result of the drug overdose. We agree that lidocaine administration, even at the conventional therapeutic dose, needs caution, especially in elderly patients with congestive heart failure and acute diaphragmatic myocardial infarction.

Atrial Diastolic Friction Rubs

THE HALLMARK of pericarditis is a pericardial friction rub. Friction rubs are commonly triphasic, consisting of atrial systole (atrial or presystolic rub), ventricular systole (systolic rub), and ventricular diastole (protodiastolic rub). Pericardial rub is generated by active motion (atrial or ventricular systole) as well as by passive motion (ventricular diastole). We have recorded the unusual condition of pericardial friction occurring during atrial diastole. We found that previous documentation of this phenomenon in the literature is limited to a single case report.1 Report of Cases Case 1.— A 72-year-old man was admitted on March 19, 1975, to the intensive coronary care unit at Rothschild Hospital in Haifa, Israel. An acute diaphragmatic myocardial infarction had developed, and ECG evidence of an anteroseptal scar was found. At the time of admission, accelerated idioventricular rhythm and transient firstand second-degree atrioventricular block were diagnosed. On March 24, a triphasic pericardial friction rub developed in

Value of the QRS complex in assessing left ventricular ejection fraction

The relation between electrocardiographic findings and the angiographic left ventricular ejection fraction and the augmented ejection fraction after a premature ventricular contraction was investigated in 73 patients with documented chronic coronary artery disease. The patients were separated into four groups according to the presence or absence of abnormal Q waves. Twenty-four patients had diaphragmatic myocardial infarction, 21 had anterior myocardial infarction, 15 had both and 13 had no myocardial infarction. There were no statistically significant differences in cardiac index, left ventricular end-diastolic pressure or number of coronary vessels showing critical narrowing in the four groups. The sum of R waves (in mv) in leads aVL, aVF and V 1 to V 6 (ΣR) was correlated with the ejection fraction (EF) and the augmented ejection fraction (EFa). EF in percent = 6.6 ΣR mv + 9.4 (no. = 73, r = 0.61); and EFa in percent = 8.6 ΣR mv + 11.0 (no. = 73, r = 0.77). Among patients with ΣR of less than 4.0 mv, augmented ejection fraction was less than 0.45 in 73 percent; among patients with ΣR of 4.0 mv or more the augmented ejection fraction was greater than 0.45 in 93 percent ( P < 0.001). Thus, the ΣR, calculated from six precordial and two augmented leads in patients with chronic coronary artery disease, correlated with both ejection fraction and augmented ejection fraction. The electrocardiogram in patients with coronary artery disease may prove useful as a simple, readily available and noninvasive guide in the assessment of left ventricular function in patients with coronary artery disease.

Relation of Heart Block and Left Ventricular Dysfunction in Acute Myocardial Infarction

Two hundred one patients with acute transmural myocardial infarction were studied to determine the relation of heart block and the degree of left ventricular dysfunction. Right bundle branch block occurred in 17, left bundle branch block in 7 and either left anterior or left posterior hemiblock in 8 patients. Hemodynamic studies were carried out before heart block developed. Complete heart block occurred in 9 of 92 patients with diaphragmatic (inferior) myocardial infarction and in 6 of 109 with anterior infarction. In patients with diaphragmatic infarction who experienced complete heart block hemodynamic measurements before block did not differ significantly from those in patients without block. Similarly, in patients who had right bundle branch block or hemiblock the hemodynamic variables did not differ from those in patients without bundle branch block. In patients with anterior infarction who experienced complete heart block, however, stroke index (<i>P</i> < 0.01) and stroke work index (<i>P</i> < 0.05) were significantly lower before block than in patients without block. Similarly, patients with anterior infarction with progression to left bundle branch block had a lower stroke index (<i>P</i> < 0.002) and stroke work index (<i>P</i> < 0.05) than patients without bundle branch block. The data indicate that patients whose anterior infarction is followed by complete heart block or left bundle branch block have a greater degree of left ventricular dysfunction than patients with anterior infarction who do not manifest these conduction defects. The profound hemodynamic derangement in the patients with these defects is probably a result of more extensive myocardial necrosis. Complete heart block after diaphragmatic infarction and right bundle branch block and hemiblock were not associated with significantly different hemodynamic measurements, thus suggesting that these conduction defects are unrelated to the extent of left ventricular dysfunction. Although only a small number of patients with heart block were studied, careful analysis of the clinical and hemodynamic data support the findings.

Vectorcardiographic diagnosis of diaphragmatic myocardial infarction

Vectorcardiograms of 31 patients with arteriographic evidence of complete occlusion of the right coronary artery were analyzed in order to evaluate and attempt to improve the vectorcardiographic criteria for the diagnosis of an old diaphragmatic myocardial infarction. The electrocardiogram showed no evidence of a diaphragmatic infarction in 48 percent of these patients. This was advantageous, since the intent of the study was to develop vectorcardiographic criteria that exceeded the capability of the electrocardiogram. The criteria that appeared optimal were: (1) an instantaneous 0.02 second QRS vector equal or superior to 315 degrees (-45 degrees) in the sagittal plane, or (2) ratio of voltages of 0 to left x-intercept to maximal QRS vector greater than 0.22 in the frontal plane. These criteria identified a diaphragmatic infarction in 77 percent of patients (24 of 31) with complete occlusion of the right coronary artery. There were no false positive findings in 40 normal subjects. A group of criteria previously defined by others, based upon rotation, contour of initial forces, duration of superior forces relative to the contour, magnitude of 0 to left x-intercept, and maximal QRS vecotr, was equally sensitive. Other previously defined criteria were less sensitive. The criteria developed in this study, when tested in 22 patients with prominent Q waves indicative of an old diaphragmatic infarction, properly diagnosed the infarction in all 22 patients. All previous criteria also successfully detected infarction in these patients. However, the new criteria identified a greater number of patients without electrocardiographic evidence of diaphragmatic infarction than were identified with previously defined vectorcardiographic criteria unless the latter were complex.

Left ventricular performance in coronary artery disease evaluated with systolic time intervals and echocardiography

Simultaneous determinations of systolic time intervals (preejection period index [PEPI], left ventricular ejection time index [LVETI] and ratio of preejection period to left ventricular ejection time [PEP/LVET]) and echographic measures of left ventricular performance (percent change in minor axis diameter [%ΔD], circumferential shortening rate [Vcf] and end-diastolic diameter [Dd]) were obtained in 25 normal subjects and 37 patients with previously documented transmural myocardial infarction. The group with previous infarction demonstrated significant ( P < 0.001) differences from the normal group in each of the noninvasive measures. PEP/LVET and %ΔD were the most sensitive measures of left ventricular dysfunction. Deviation from the normal range in these measures occurred, respectively, in 70 and 65 percent of patients without dyspnea or fatigability (20 patients) and in 85 percent of those without angina pectoris (13 patients). Abnormalities in systolic time interval and echocardiographic measures were related to the severity of dyspnea and fatigability but not to that of angina. Neither the presence of phonocardiographically documented third or fourth sound gallops nor an abnormal cardiothoracic ratio by chest roentgenogram reliably detected patients with abnormal left ventricular performance. The range of abnormality in left ventricular performance did not differ between patients with prior anterior or diaphragmatic myocardial infarction. The frequency of abnormal performance was greatest among patients with combined sites of prior infarction. Among 26 patients studied by coronary arteriography, abnormal left ventricular performance as determined by values for PEP/LVET and %ΔD occurred in fewer than 30 percent of those with 70 percent or greater obstruction of one coronary artery and in more than 80 percent of those with two or three vessel involvement. There was a high correlation between systolic time intervals, %ΔD and Vcf, the closest correlation occurring between PEP/LVET and %ΔD ( r = −0.93). These data document the sensitivity of the noninvasive systolic time intervals and echographic measures and their superiority over current clinical bedside methods in evaluating left ventricular performance in patients with prior myocardial infarction.

Lead Thirteen Electrocardiography

To the Editor.— In a LETTER TO THE EDITOR (224:1533, 1973) entitled " `Lead Thirteen' Electrocardiography," Dr. Sanford Lewis makes a plea for the routine recording of lead III during deep inspiration to differentiate between abnormal Q waves indicating diaphragmatic infarction and benign Q waves. Q waves persisting during inspiration are regarded as due to diaphragmatic infarction. We disagree with this recommendation. In our experience this maneuver has not been helpful in distinguishing abnormal Q waves due to diaphragmatic myocardial infarction from benign Q waves. A Q wave is considered abnormal if it is 0.04 seconds or more in duration and at least 25% of the QRS voltage (amplitude) It is true that in many individuals a Q wave in lead III may disappear or become insignificant on deep inspiration. This, however, does not always establish the benign nature of the Q wave, since a marked number of patients with well-established

Significance of high degree atrioventricular block in acute posterior myocardial infarction. The importance of clinical setting and mechanism of block.

This report evaluates the morbidity and mortality, during hospitalization and follow-up, of a subgroup of patients with posterior or diaphragmatic myocardial infarction (PDMI) who developed high degree A-V block via a type I mechanism and in the absence of power failure (pulmonary edema or cardiogenic shock). This subgroup was not at any higher risk of hospital morbidity, hospital mortality, or 1-year mortality than three other groups: (a) patients with PDMI but neither high degree A-V block nor initial power failure; (b) patients with other infarct sites who developed high degree A-V block in the absence of power failure; and (c) patients with other infarct sites but neither high degree A-V block nor initial power failure. The significance of subgrouping patients with high degree A-V block by the quantity of clinical heart failure is exemplified by a review of the literature and the present study.

Intermittent Heart Block Related to Treatment of Hypertension in a Patient with Acute Myocardial Infarction

A patient with an acute diaphragmatic myocardial infarction and persistent hypertension developed varying degrees of A-V block including complete heart block as his blood pressure was lowered. Block could be abolished by allowing the blood pressure to rise. His bundle electrograms during heart block demonstrated the conduction defect to be proximal to the His bundle in the A-V node. The patient was managed with a stand-by demand pacemaker that allowed safe normalization of his blood pressure.

Site of heart block in acute myocardial infarction.

Bundle of His electrograms were recorded in eight patients with acute myocardial infarction and heart block. Three patients with diaphragmatic myocardial infarction (DMI) and one with subendocardial infarction were characterized by slowing or block above the bundle of His and A-V junctional escape rhythms during periods of advanced or complete block. An additional patient with DMI had block in the His bundle itself. Intraventricular conduction in the above patients was characterized by normal H-Q intervals (35 to 60 msec) and absence of widened QRS. In contrast, three patients with anterior infarction (AMI) manifested complete block below the bundle of His and idioventricular escape. P-H intervals were normal (80 to 140 msec) and A-V conduction was considered unaffected. Our electrophysiologic observations coupled with previous clinical, anatomic, and pathologic findings suggest that the heart block in DMI is usually due to an ischemic lesion of the A-V node, while heart block in AMI is due to necrosis involving both bundle branches.

Coronary Arteriographic and Ventriculography Correlations with the ECG Diagnosis of Diaphragmatic Myocardial Infarction (DMI).

Excerpt To more accurately determine the value of the electrocardiogram (ECG) in diagnosing coronary artery disease, 48 patients with a history of chest pain and ECG evidence of diaphragmatic myoca...

Unusually Marked Sinus Arrhythmia as a Complication of Acute Diaphragmatic Myocardial Infarction

An instance of markedly irregular sinus arrhythmia associated with acute diaphragmatic myocardial infarction has been described. It is quite unusual to observe an extreme sinus arrhythmia in an adult without the intervention of A-V nodal or ventricular escape rhythm.The influence of digitalis, reserpine, guanethidine and morphine in relation to such cardiac arrhythmia has been discussed.Sinus arrhythmia and/or sinus bradycardia are usually transient and require no treatment unless cardiac output is compromised. This arrhythmia may be mistaken for more serious arrhythmias such as A-V block, S-A block and sinus arrest because of marked irregularity with slowing of the heart rate.

Advanced heart block as a complication of acute myocardial infarction. Role of pacemaker therapy

The association of advanced or complete heart block with acute myocardial infarction was reviewed as a basis for understanding the special problems related to the complicating heart block and for evaluating artificial cardiac pacemaker therapy in this disease. In addition to studies reported in the literature, 28 personal cases of advanced heart block with acute myocardial infarction were analyzed. The average reported incidence of second degree heart block was 5 percent and of complete heart block 3 percent of cases of acute myocardial infarction; but in patients who were continuously monitored, a higher incidence was noted-fiz., 10 percent for second degree block and 8 percent for complete heart block Since the atrioventricular node and bundle are supplied by the right coronary artery in 90 percent of persons, advanced heart block occurs chiefly with acute diaphragmatic infarction. When advanced heart block occurs with anterior myocardial infarction, there is usually severe narrowing or old occlusion of the right coronary artery as well as a fresh occlusion of the left coronary artery. There is usually extensive septal infarction causing bilateral branch block. The fatality rate is much higher in cases of advanced heart block with anterior than with diaphragmatic myocardial infarction. In patients who recover, chiefly those with diaphragmatic infarcts, the heart block usually disappears, indicating that the heart block was due to reversible ischemia of the artrioventricular node. In fatal cases of advanced heart block with diaphragmatic infarction, there is evidence of severe left coronary narrowing or occlusion as well as occlusion of the right coronary artery. The fatality rate is determined not only by the complicating heart block, as such, but also by the location of the infarct, the type of the idioventricular QRS complex in complete heart block, and especially by other associated complications such as shock and heart failure. The prognosis is more favorable with diaphragmatic than with anterior myocardial infarction, with a narrow, “supraventricular type” of QRS complex than with a wide, “aberrant” idioventricular QRS complex, and in the absence of serious complications. Reports of fatalities in various series of cases with and without any particular therapy must be analyzed with proper regard for these prognostic factors. In our series of 28 cases, there were only two deaths among nine patients with diaphragmatic infarction and narrow QRS complexes, five deaths among seven patients with diaphragmatic infarction and wide QRS complexes and seven deaths among eight patients with advanced or complete heart block and acute anterior myocardial infarction. In four patients with advanced heart block and subendocardial infarction, there were no deaths. The insertion of a temporary transvenous cardiac pacemaker has been advocated for the treatment of heart block complicating acute myocardial infarction in the belief that (1) heart block is responsible for a higher mortality than would otherwise occur in similar cases without heart block and (2) that pacemaker insertion during the acute phase of heart block reduces this excess mortality. Although these beliefs seem valid, reported data are inadequate to conclude that increased mortality is due to the heart block per se, and not to other serious complications which themselves are associated with a high fatality rate. Actually, the fatality rate has been high in reported series of cases in which pacemakers were inserted, but the poor results were undoubtedly due in large measure to the poor condition of many of the patients. Failure to classify cases in terms of other factors besides heart block which might influence prognosis impairs any conclusion as to the value of pacemakers in heart block with myocardial infarction and as to the precise indications for their use. Nevertheless, continued application of this form of therapy, with careful analysis in terms of the various known prognostic factors, appears justified.

Congenital right coronary artery to left atrium fistula ∗

The first case of connection of a branch of the right coronary artery with the left atrium is presented. This branch is probably the sinus node artery. 26 Only 6 cases of fistula from a coronary artery to the left side of the heart were found in the literature; all involved the left coronary artery. This is also the first time that a fistula from a coronary artery to the left heart chamber has been recognized preoperatively and the anatomic details established by cineangiocardiography. Mitral regurgitation was present prior to surgery, and its possible etiology is discussed. Ligation of the abnormal vessel was followed by development of diaphragmatic myocardial infarction. Selective coronary cinearteriography postoperatively demonstrated a large collateral flow from the left coronary artery into the irfarcted area.