Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Isolated atrial infarction in a patients with single vessel disease of the sinus node artery

Atrial infarction is found in approximately 17 percent of autopsy-proven cases of myocardial infarction, but is a frequently missed clinical diagnosis. The antemortem diagnosis of atrial infarction occurring in the absence of ventricular infarction has not been previously reported. We present a patient with ischemic chest discomfort associated with paroxysmal atrial fibrillation. Electrocardiographic and enzymatic changes were consistent with atrial infarction. Cardiac catheterization demonstrated single vessel critical stenosis at the origin of the sinus node artery. Combined atrial and ventricular infarction occurs frequently and should be considered in the setting of paroxysmal supraventricular arrhythmias occurring early in the course of ventricular myocardial infarction. Lone atrial infarction is a rare but distinct clinical entity. The tetrad of typical ischemic chest discomfort, paroxysmal supraventricular arrhythmia, P-Ta segment shifts, and elevated cardiac enzyme levels without evidence for ventricular infarction strongly suggests isolated atrial infarction.     

Severe bradycardia following electrical cardioversion for atrial tachyarrhythmias in patients with acute myocardial infarction

Bradycardia following electrical cardioversion is an uncommon complication. The present report describes three patients who developed life-threatening bradycardia following electrical cardioversion for atrial tachyarrhythmias in the setting of an acute myocardial infarction. All three patients had multivessel coronary artery disease with a totally occluded right coronary artery and a possibility of ischemic sinus node dysfunction. When electrical cardioversion is undertaken for new onset of atrial tachyarrhythmia in the setting of an acute myocardial infarction, measures for immediate, temporary pacing should be easily available.     

A clinical angiographic study of the arterial blood supply to the sinus node

We studied the arterial blood supply to the sinus node area in 309 consecutive patients undergoing coronary arteriography. Seventy-nine had had a previous myocardial infarction. In two who developed temporary sinus node dysfunction, the sinus node artery arose from the distal portion of a severely stenotic left circumflex coronary artery, but in 307 of the 309 patients the sinus node arteries themselves were free of atheroma. The sinus node artery arose from the right coronary artery in 182 patients, from the proximal 3 cm in 179, near the origin of the acute marginal in one, and left of the crux in two. In 119 patients it arose from the left circumflex coronary artery, proximally in 87, and in 32 from anywhere throughout its length, running posteriorly as the posterior sinus node artery. Finally, eight patients had two sinus node arteries, one arising from the right coronary artery and one from the left circumflex.     

Significance of ST segment depression during paroxysmal supraventricular tachycardia

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死患者Ⅲ度房室传导阻滞与房室结动脉血供的关联性

目的 观察和分析急性心肌梗死(AMI)患者Ⅲ度房室传导阻滞(AVB)与房室结动脉血供的关系。方法 将入选的AMI患者,按是否并发Ⅲ度AVB分为两组:病例组为AMI并发Ⅲ度AVB的患者（n=35例）,对照组为AMI未并发Ⅲ度AVB的患者（n=215例）,通过观察梗死相关动脉并分析房室结动脉血供来源情况,分析AMI患者不同房室结动脉血供来源发生Ⅲ度AVB的几率,并观察AMI并发Ⅲ度AVB的患者,房室结动脉血运改善后Ⅲ度AVB恢复时间。结果 房室结动脉血供来源于右冠状动脉的右上降支动脉和回旋支的kugel’s动脉之一或二者双重血供。病例组患者,其房室结动脉血供仅来源于右冠状动脉的右上降支或回旋支的kugel’s动脉,无前降支来源,并且右冠状动脉较回旋支多见（P<0.01）。当梗死相关动脉得到再灌注,恢复血运后,AVB均恢复到窦性心律。结论 急性心肌梗死Ⅲ度AVB发生患者与其房室结动脉血供中断有关,恢复房室结动脉血供后AVB恢复窦性心律。     

Anomalous origin of right coronary artery from left coronary sinus

Anomalous aortic origin of the coronary arteries is uncommon but clinically significant. Manifestations vary from asymptomatic patients to those who present with angina pectoris, myocardial infarction, heart failure, syncope, arrhythmias, and sudden death. We describe 4 patients, aged 34 to 59 years, who were diagnosed with right coronary artery arising from the left sinus of Valsalva, confirmed by coronary angiography, which was surgically repaired. Three patients presented dyspnea and angina, and one with acute myocardial infarction. At operation, the right coronary artery was dissected at the take-off from the intramural course, and reimplanted into the right sinus of Valsalva. There was no mortality. One patient had associated coronary artery disease that required stent placement postoperatively. This reimplantation technique provides a good physiological and anatomical repair, eliminates a slit-like ostium, avoids compression of the coronary artery between the aorta and the pulmonary artery, and gives superior results to coronary artery bypass grafting or the unroofing technique.     

Peri-operative supraventricular arrhythmias in coronary bypass surgery

One hundred consecutive admissions for coronary bypass surgery were studied to establish the incidence of peri-operative supraventricular arrhythmias, to monitor their evolution, and to identify their possible aetiological factors. No important arrhythmias were detected before the operation. Post-operatively, 24 patients (24%) developed supraventricular arrhythmias. Nineteen of them had atrial fibrillation or flutter (19%), 2 had supraventricular tachycardia (2%), and 3 had inappropriate sinus bradycardia (less than 45 min) (3%). Almost two-thirds of the arrhythmias occurred within the critical early post-operative period (63%). Haemodynamic compromise ushered the onset of arrhythmias in more than one-third of the patients in whom antiarrhythmic measures ensured prompt improvement (37.5%). Three-quarters of those with atrial fibrillation or flutter were back in sinus rhythm at the time of discharge from hospital (74%). The incidence of supraventricular arrhythmia was significantly higher in patients with demonstrable myocardial ischaemia prior to surgery, in patients who underwent adjunctive coronary endarterectomy, or in those in whom topical cardiac cooling was applied (50%, 45%, and 58%, respectively). Supraventricular arrhythmias are frequently encountered during the critical early post-operative period when serious but reversible haemodynamic compromise might be precipitated. Although the nature of the underlying myocardial insult remains obscure, supraventricular arrhythmia may be related more to defective myocardial preservation than to any specific underlying myocardial lesion.     

Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.

The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery.     

Etiology of the negative chronotropic responses to transient coronary artery occlusion in the anesthetized rhesus monkey.

Etiology of the negative chronotropic response to coronary artery occlusion was studied in chloralose-anesthetized monkeys. One-minute occlusion of the circumflex (CIRC) coronary artery resulted in marked negative chronotropic responses and consistent alterations in atrial electrograms. These responses were dependent on interruption of flow to a small proximal CIRC branch, and postmortem examination revealed that it perfused the sinus node region. The negative chronotropic response was not dependent on any apparent neural reflexes because it was not affected by autonomic blockade. Coronary artery occlusion in anesthetized monkeys can result in significant decreases in heart rate and changes in atrial electrical activity when flow to the pacemaker region is interrupted. We suggest that (1) rhesus monkeys may be suitable for study of the sick sinus syndrome, and (2) atropine-resistant bradycardia and atrial arrhythmias observed in postinfarction patients may be due to sinus node artery blockade.     

Clinical, angiographic, and hemodynamic findings in patients with anomalous origin of the coronary arteries.

Clinical and angiographic features of 31 patients with anomalous coronpary artery origin are reviewed. Of 17 aberrant circumflex arteries from the right sinus of Valsalva or artery, each was retro-aortic, six atherosclerotic, and seven irrigated a small area of myocardium. Of seven anomalous right coronary arteries from the left sinus of Valsalva or artery, each was ante-aortic and two atherosclerotic. Aberrant origin of the circumflex or right coronary artery was a benign anomaly. The proximal course of seven aberrant left coronary arteries from the right sinus of Valsalva or right coronary artery was related to clinical events. The anomaly was best demonstrated in the lateral view. In five cases, coronary blood flow during exercise and myocardial metabolism during pacing were assessed. Two had had a previous infarction with nonatherosclerotic arteries. Exercise coronary blood flow was normal in four and low in one patient. Pacing resulted in lactate production in two with atherosclerotic and one without atherosclerotic arteries. We conclude that anomalous left coronpary origin from the right sinus of Valsalva can result in significant myocardial ischemia and infarction.     

Anatomical Reasons for the Discrepancies in Atrioventricular Block after Inferior Myocardial Infarction with and without Right Ventricular Involvement

The incidence of arrhythmias after acute myocardial infarction of the inferior wall varies with the affected segment and increases when there is right ventricular involvement. This paper provides a clear review of the blood supply to the conduction system and gives an anatomic explanation of that supply.We dissected 20 human hearts after anterograde and retrograde injection of latex. In every heart, we dissected the conduction system and its blood supply. Retrograde perfusion enabled proper injection of the atrial vessels that originate at the beginning of the coronary trunks.We describe the 4 main arteries that supply blood to the conduction system. The classic concept included the atrioventricular node artery and the 1st septal artery. To that we add Kugel''s artery and the right superior descending artery.The incidence of arrhythmias after acute myocardial infarction of the inferior wall is greater when the occlusion of the coronary trunk is at or near the origin. This is due to the existence of the right superior descending artery, which is given off by the right coronary trunk less than 1 cm from the origin. The arrhythmias caused by the occlusion of the circumflex artery are due to the existence of Kugel''s artery, which displays a peculiar anastomotic pattern.Key words: Atrioventricular node, cadaver, coronary vessels/anatomy & histology, heart atria, heart block/etiology, humans, heart conduction system, myocardial infarction, inferior/complicationsArrhythmias as a complication of acute myocardial infarction of the inferior wall vary in their occurrence, depending on the presence or absence of right ventricular involvement.^1–3 Many articles have made this observation, but, to the best of our knowledge, none has offered a clear morphologic explanation: that is, there have been few images of the heart''s conduction system, particularly of the blood supply to the conduction system in the atrioventricular (AV) node and of the alternative blood supply to that conduction system (which has been shown in drawings and diagrams, but not in photographs). This paper reviews our present knowledge of the blood supply to the conduction system and supplements it with new findings that help to explain why the incidence of postinfarction arrhythmias is greater when there is right ventricular involvement. Two atrial arteries have been described⁴ by the authors as sources of the blood supply to the conduction system: Kugel''s artery (arteria anastomotica auricularis magna) and the right superior descending artery. These vessels, which appear to constitute the chief explanation for the phenomenon mentioned above, are thoroughly discussed herein.     

Chronic sinoatrial disorder (sick sinus syndrome): a possible result of cardiac ischaemia.

Postmortem angiography was used to examine the blood vessels supplying the sinoatrial node in 25 subjects with chronic sinoatrial disorder (group 1). The results were compared with similar studies in 54 subjects who died of heart block and in whom sinus node function was normal (group 2). Although no significant lesion obstructing the blood flow to the sinus node was seen in the majority of those in group 1, there were abnormalities in seven cases, with reduced filling of the sinus node artery in five. In group 2 the sinus node artery filled normally in all cases despite major disease of the parent vessel in three. The combination of contralateral coronary artery disease with extensive atrial anastomoses was actively sought because this arrangement might predispose to a steal phenomenon. Such conditions were fully met in three cases in group 1 and two cases in group 2, and were found to a lesser extent in a further two cases in group 1 and three in group 2. Although coronary artery disease was unlikely to be the principal cause of sinus node dysfunction in most of the cases studied it was relatively common and may have been a factor in about one third. Improved survival after myocardial infarction may increase the number of patients with chronic sinoatrial disorder of ischaemic origin.     

Sinus node dysfunction in acute myocardial infarction.

The frequency, clinical course, and prognosis of sinus node dysfunction in 431 patients with acute myocardial infarction admitted to the coronary care unit were studied. Sinus node dysfunction occurred in 20 patients. In 13, the principal manifestation consisted of severe sinus bradycardia. In the remaining 7, periods of bradycardia alternating with episodes of supraventricular tachycardia were noted. Though several of the patients with sinus bradycardia required intravenous atropine or temporary pacing, normal sinus rhythm returned in virtually all during follow-up. The clinical course of patients with both bradycardia and tachycardia was less benign, during the acute phase and during follow-up; 5 of the 6 survivors required continued antiarrhythmic therapy or permanent pacing. The differences in the clinical course between these two groups of patients may reflect distinct underlying pathological changes. The findings in this study suggest that in contrast to sinus bradycardia, the occurrence of bradycardia-tachycardia syndrome during the acute phase of myocardial infarction may have important prognostic implications.     

Sinus node dysfunction in acute myocardial infarction.

The frequency, clinical course, and prognosis of sinus node dysfunction in 431 patients with acute myocardial infarction admitted to the coronary care unit were studied. Sinus node dysfunction occurred in 20 patients. In 13, the principal manifestation consisted of severe sinus bradycardia. In the remaining 7, periods of bradycardia alternating with episodes of supraventricular tachycardia were noted. Though several of the patients with sinus bradycardia required intravenous atropine or temporary pacing, normal sinus rhythm returned in virtually all during follow-up. The clinical course of patients with both bradycardia and tachycardia was less benign, during the acute phase and during follow-up; 5 of the 6 survivors required continued antiarrhythmic therapy or permanent pacing. The differences in the clinical course between these two groups of patients may reflect distinct underlying pathological changes. The findings in this study suggest that in contrast to sinus bradycardia, the occurrence of bradycardia-tachycardia syndrome during the acute phase of myocardial infarction may have important prognostic implications.     

Atrial natriuretic factor in acute atrial hyperkinetic arrhythmia and chronic atrial fibrillo-flutter

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.     

Incomplete myocardial rupture after coronary embolism of an isolated single coronary artery.

An 82-year-old female was admitted to the coronary care unit with an anterior wall myocardial infarction and cardiogenic shock. She was in chronic atrial fibrillation without oral anticoagulation. Coronary angiography showed occlusion of the left main coronary artery which originated together with a normal right coronary artery from the right sinus of Valsalva. The advanced age, the presence of chronic atrial fibrillation not anticoagulated and the normal appearance of the remaining coronary arteries suggested a thromboembolic origin. Transthoracic echocardiography showed an abrupt interruption of the myocardial wall, in the apical portion of the interventricular septum, not communicating with the pericardial sac or right ventricular cavity suggesting the presence of an incomplete contained rupture of the myocardial wall at this location. She died in cardiogenic shock due to the extensive left ventricular damage.     

The effect of atropine on cardiac arrhythmias and conduction. Part 2

The effects of atropine on various components of the specialized conduction system of the heart and the myocardium itself are reviewed. These actions are sometimes unpredictable or paradoxical, depending on the component showing the dominant effect and the health of the entire system. Atropine is best known for its chronotropic effect. Improved sinoatrial conduction has been demonstrated but the effect on the refractoriness of atrial muscle is unsettled. Atropine stimulates the atrioventricular (A-V) junctional pacemaker and facilitates conduction through the A-V node. The response of the subjunctional portion of the specialized conduction system to the drug is unpredictable and controversial in some respects.Atropine is useful in the diagnosis of sinus node dysfunction, in the evaluation of coronary artery disease during atrial pacing, and in attempting to produce normal conduction in patients with the Wolff-Parkinson-White Syndrome. Its principal therapeutic application is in correcting the hypotension-bradycardia syndrome occurring during acute myocardial infarction. It also has a role in the temporary management of sinus node dysfunction. Atropine may also cause arrhythmias, including atrial fibrillation, A-V dissociation, ventricular tachycardia, and ventricular fibrillation. The clinical settings in which atropine may be arrhythmogenic are discussed.     

Angioplasty in total coronary artery occlusion

Percutaneous transluminal coronary angioplasty was attempted without streptokinase in 24 patients with total coronary artery occlusion but without acute transmural myocardial infarction. The maximal duration of occlusion was estimated to be 1 week or less in 10 patients, more than 1 to 4 weeks in 6, more than 4 to 12 weeks in 3 and more than 12 weeks in 5. Dilation of the occluded artery was attempted in the left anterior descending coronary artery in 17 patients, in the right coronary artery in 4 and in the circumflex coronary artery in 3. Angioplasty was successful in 13 patients (54%): left anterior descending coronary artery in 59%, right coronary artery in 50% and circumflex coronary artery in 33%. In patients with successful dilation, there was a mean decrease in coronary artery stenosis from 100 to 23%. In the 19 patients whose occlusion was estimated to be of 12 weeks' duration or less, angioplasty was successful in 68%. In the five patients whose occlusion was estimated to be of more than 12 weeks' duration, dilation was not successful in any (p = 0.006). It is concluded that in selected patients with symptomatic coronary artery disease and recent coronary artery occlusion without associated acute myocardial infarction, percutaneous transluminal coronary angioplasty alone may be effective in restoring patency.     

Stability of AV conduction in sick sinus node syndrome patients with implanted atrial pacemakers

Single-chamber atrial pacing is effective in the management of sinus node dysfunction, subject to the uncertainty of long-term atrioventricular conduction. Despite the accepted observation that many patients with sinus node dysfunction also have atrioventricular conduction disease, data do not exist on the development of atrioventricular block in those patients with permanent single-chamber atrial pacing. Of 70 patients who received single-chamber atrial pacing from 1967 to 1982 (mean duration of pacing was 33 months), only two patients of 58 (3.4%) of those with sinus node dysfunction developed atrioventricular (AV) block—after 14 months in one patient and after 23 months of successful atrial pacing in the other. None of the 12 patients paced for tachyarrhythmia management developed AV block. Of the 70 patients, 37 had assessment of AV conduction by incremental atrial pacing at the time of implant and 20 patients underwent atrial pacing on the basis of surface ECG and clinical judgment. Electrophysiologic studies were conducted only in those patients being paced for control of supraventricular arrhythmias. Only 5 of the 70 patients required conversion to ventricular pacing for technical difficulties; three of these conversions occurred in the early 1970's before the advent of atrial tined or J leads; one was for irreparable lead fracture and only one occurred in a patient with a newer design atrial lead. In conclusion, progression to AV block in patients with permanent atrial pacing is uncommon; formal electrophysiologic studies are necessary mainly in patients with supraventricular arrhythmias; and in the majority of patients, AV conduction can be assessed at the time of implant. Continued improvement in atrial leads should make atrial pacing even more successful.