Ventricular arrhythmias in ischemic heart disease

Ventricular arrhythmias remain the leading cause of death from coronary artery disease. This review summarizes current thinking in several areas relating to the pathophysiology, prognosis, and therapy of ventricular arrhythmias associated with acute and chronic coronary artery disease syndromes. The experimental basis of arrhythmias in the setting of acute myocardial ischemia and chronic myocardial infarction is described, stressing the important pathophysiologic differences between these two conditions. The effects of the autonomic nervous system as a key modulator of ischemic arrhythmogenesis are discussed. Insights, derived from endocardial mapping studies, into the nature of ventricular tachycardia in humans with chronic myocardial infarction are described, including implications for risk stratification and therapy to prevent arrhythmia recurrence. Current therapeutic principles are discussed in the management of ventricular arrhythmias associated with coronary artery disease, including pharmacologic approaches, surgical and catheter ablation, and automatic implantable cardioverting and defibrillating devices.     

Noninvasive assessment of ventricular arrhythmias in clinical practice: prognostic implications

Frequency and complexity of ventricular arrhythmias increases with age and increasing severity of heart disease. However, fatal ventricular fibrillation occurs frequently in the absence of symptomatic warning arrhythmias. Several classifications of ventricular arrhythmias are discussed. The morphology of ventricular premature complexes (VPC), their frequency and complexity at rest, during ordinary activity, or after exercise do not influence life expectancy of subjects without heart disease, nor in those with coronary artery disease with no history of myocardial infarction. In the survivors of myocardial infarction, the frequency and "complexity" of ventricular arrhythmias appears to be an independent risk factor for sudden and nonsudden cardiac death. However, the low specificity and predictive value of ventricular arrhythmias makes their assessment difficult for practical purposes. The prognosis of most patients with ventricular arrhythmias is determined predominantly by the condition of the heart. "Complex" arrhythmias at rest and during exercise do not appear to worsen prognosis and life expectancy in individuals without heart disease. Ambulatory electrocardiographic monitoring has serious limitations as a guide for clinical decision making. Ventricular tachycardias in patients with coronary artery disease are not strictly related to the frequency and "complexity" of ventricular premature complex, but correlate with the presence of ventricular aneurysms, poor ventricular function and late potentials in the signal-averaged high frequency electrocardiogram. Recording of such late potentials is a new and promising noninvasive technique for identification of patients with serious arrhythmias but the sensitivity and specificity of this method remains to be established.     

Bundle branch block and sudden death

It is clear from the available data that the prognosis for patients with chronic BBB depends to a large extent on the presence and etiology, as well as the severity, of the associated heart disease. In most patients, the terminal event is usually one of heart failure or the complication of coronary artery disease. In the absence of clinically detectable heart disease, the long-term prognosis for this group of patients is good.Patients with chronic bundle branch block Have been shown to have an incidence of ventricular arrhythmias greater than that found in a normal population. The mechanism of sudden death in any single unmonitored patient is speculative. Most patients dying suddenly, especially those with coronary artery disease, probably do so from ventricular fibrillation. Patients with documented transient high-degree AV block are at a substantial risk of sudden death.No clinical variable (such as age, syncope, angina, shortness of breath), or physical finding (such as S₃ gallop, cardiomegaly, heart failure), or electrocardiographic finding (such as RBBB with LAD, RBBB with RAD, P-R interval prolongation), or electrophysiologic variable (such as A-H or H-V interval prolongation) is useful in predicting progression to complete heart block. All the above variables occur frequently in patients with BBB and yet the progression to CHB is relatively infrequent. One might single out His-Purkinje block with normal AV nodal conduction during atrial pacing as a possible marker for development of complete heart block. However, the opposite, namely a normal H-V interval, does not rule out progression to complete heart block.The data available on the use of pacing in patients with unexplained recurrent syncope or dizziness suggests that this approach is reasonable provided an effort has been made to exclude noncardiac cause for the symptoms. Some suggest that documentation of bradyarrhythmia or measurement of H-V interval is essential prior to institution of pacing. Further studies are needed to clarify this point.BBB complicating acute myocardial infarction places the individual at significant risk of developing congestive heart failure, with mortality usually secondary to myocardial failure or refractory ventricular arrhythmias. The pressence of high-degree AV block per se does appear to increase the mortality in patients without pump failure. Recent data suggest that immediate survival may be enhanced by prophylactic pacing in patients at high risk for abrupt complete heart block complicating acute myocardial infarction, but who do not manifest evidence of heart failure. The assumption that prophylactic pacing will improve survival of patients with bundle branch block and significant heart failure complicating acute myocardial infarction is purely speculative.Insufficient and conflicting data prevent a definitive statement regarding the usefulness of the P-R and H-V intervals as guidelines for the management of patients with recent-onset bundle branch block and acute myocardial infarction.Permanent pacing appears to benefit survivors of acute myocardial infarction complicated by BBB and transient high-degree AV block. However, the evidence is far from convincing.Little information is available on the influence of antiarrhythmic therapy on sudden death in patients with BBB. All currently used antiarrhythmic agents have a potentially high risk when administered to patients with BBB. Since there is no convincing prospective study as to the efficacy of drugs in preventing sudden death in patients with BBB, drug selection and its use in this group of patients remains at the discretion of the individual physician. It is based on the individual physician's experience with the drug in question and his perception of the benefit-to-risk ratio of the agent to be used.     

A perspective on ventricular arrhythmias: patient assessment for therapy and outcome

Clinical management of patients with ventricular arrhythmias continues to evolve. It is generally accepted that patients with sustained ventricular tachyarrhythmias (ventricular tachycardia [VT] or fibrillation) require treatment. It is also generally accepted that patients with frequent or complex ventricular ectopy or nonsustained VT, in the absence of underlying heart disease, do not require treatment unless relief of symptoms is warranted. Whether patients with frequent or complex ventricular ectopy or nonsustained VT require treatment in the presence of underlying organic heart disease remains uncertain. The concern is that these ventricular arrhythmias may be a precursor for sustained, potentially life-threatening ventricular tachyarrhythmias. Available data suggest that patients with underlying heart disease, particularly coronary artery disease and a previous myocardial infarction, who manifest frequent or complex ventricular ectopy or nonsustained VT are at increased risk for sudden cardiac death. However, no studies have shown that treatment of these arrhythmias will affect outcome. Data are accumulating to suggest that use of the principles of risk stratification permits identification of patients at very high risk for developing sustained ventricular tachyarrhythmias. Carefully designed clinical trials are required before one can provide firm guidelines for the management of these patients. Nevertheless, when several risk factors for sudden cardiac death (e.g., abnormal ejection fraction, a late potential on a signal-averaged electrocardiogram, and frequent or complex ventricular ectopy or nonsustained VT) are present in a patient, especially after a recent myocardial infarction, invasive electrophysiologic testing may help identify those who need treatment (sustained VT is inducible) and those who do not (no sustained VT is inducible).     

Treatment of Chronic Myocardial Ischemia: Rationale and Treatment Options

A rational approach to the treatment of chronic myocardial ischemia requires an appreciation of the pathophysiology of coronary artery disease and the treatment options available. Any factor that causes an imbalance between myocardial oxygen supply and demand can provoke ischemia. Myocardial oxygen requirements rise with increases in heart rate, contractility, or left ventricular wall stress. Myocardial oxygen supply is determined by coronary artery flow and myocardial oxygen extraction. Anti-anginal medications are the mainstay of anti-ischemic management and act to correct the balance between myocardial supply and demand by increasing coronary blood flow, reducing myocardial oxygen requirements, or both. These medications include nitrates (which act principally by venous vasodilation, but also probably by coronary dilation), beta-blockers (which act mainly by reducing heart rate and cardiac contractility), and calcium channel blockers (which act principally by arterial and coronary vasodilation). The choice of therapy and its effectiveness depend on the underlying cause of ischemia. The complimentary mechanisms of action of these drug classes suggest that their use in combination may result in a greater reduction in myocardial oxygen demand than that achieved with monotherapy. In addition, the pharmacological actions of some of these drugs may serve to offset the undesirable side effects associated with others, for example, the reflex tachycardia produced by some calcium channel blockers may be offset by beta-blocker therapy. Finally, aspirin and lipid-lowering drugs and the potential role for anti-oxidants must also be considered in combination therapy. Invasive techniques for myocardial ischemic management, such as coronary artery bypass and coronary angioplasty, improve myocardial oxygen supply by relieving or circumventing the atherosclerotic obstruction responsible for ischemia. Surgery is the preferred technique in patients with certain medical condi tions, for example, those with triple-vessel disease, but is not recommended in patients with mild angina unless left main artery disease is present.     

Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of 9 patients with progressive systemic sclerosis

The syndrome of angina pectoris or acute myocardial infarction without obstructive coronary artery disease has been the subject of much interest. We studied nine autopsied patients with progressive systemic sclerosis and evidence of ischemic heart disease but morphologically normal coronary arteries. Three patients had angina pectoris and three others chest pains of unknown etiology, six had ventricular arrhythmias, four had clinically suspected acute myocardial infarction, and eight had sudden cardiac death. At autopsy extensive focal myocardial necrosis was present in seven patients and myocardial scarring in all nine, but all patients had widely patent intramural and extramural coronary arteries. The finding of contraction band myocardial necrosis in seven of the eight patients who experienced sudden death suggests that the myocardial damage was a consequence of reperfusion of focally nonperfused myocardium, and thus due to a myocardial Raynaud's phenomenon. Patients with PSS may provide a model of spasm of intramyocardial vessels causing angina pectoris or myocardial infarction with morphologically normal coronary arteries.     

Acute myocardial ischemia and ventricular arrhythmias in the pathogenesis of sudden cardiac death in coronary disease

There is increasing evidence for a fatal interaction of myocardial ischemia, ventricular arrhythmias and sudden cardiac death in some patients with coronary artery disease. Evidence comes from autopsy studies, from the evaluation of patients who survived an episode of sudden cardiac death, from follow-up data of these patients either treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and indicate that reducing the individual ischemic burden will be beneficial to reduce the incidence of sudden cardiac death. Studies in patients with stable and especially with unstable angina using Holter monitoring could demonstrate that there is a close and causal relationship between myocardial ischemia inducing or aggravating life-threatening ventricular arrhythmias and sudden cardiac death particularly in patients with unstable and postinfarction status. This review summarizes some of our clinical knowledge on this topic and indicates that preventive strategies for myocardial ischemia are the antiarrhythmic treatment of choice in patients with severe coronary artery disease and patients with evidence or at risk for ischemic proarrhythmia.     

Relation of silent myocardial ischemia to ventricular arrhythmias and sudden death

Silent myocardial ischemia is common in the clinical spectrum of coronary disease. Ambulatory electrocardiographic monitoring has provided the most objective evidence of silent ischemia, but the phenomenon has also been detected in patients with coronary artery disease through analysis of exercise-induced ischemic ST-segment alterations, scintigraphic myocardial perfusion defects and left ventricular wall motion abnormalities. Silent myocardial ischemia frequently occurs in patients with stable angina, unstable angina, myocardial infarction and completely asymptomatic coronary artery disease. In each of these groups, silent ischemia has been associated with an increased risk of subsequent cardiac events. However, it remains unclear whether silent ischemia is directly involved in the occurrence of these events, possibly by provoking ventricular arrhythmias. Only limited data are available on the relation between silent ischemia and arrhythmias in myocardial infarction, vasospastic angina, coronary angioplasty, exercise testing and ambulatory electrocardiography. However, fortuitous ambulatory monitoring coincident with sudden death has detected ischemia associated with lethal arrhythmias in some individual cases. This suggests that an ischemia-arrhythmia association may be important in certain patients at certain times, possibly in combination with other factors.     

Silent myocardial ischemia during daily activities: studies in asymptomatic patients and those with various forms of angina

Asymptomatic subjects with proven coronary artery disease, including those with no previous manifestations of coronary heart disease and those with previous myocardial infarction, have silent ischemic episodes during daily activity. Patients with all forms of angina, stable effort and unstable rest angina, and those with coronary artery spasm have very frequent episodes of silent myocardial ischemia during ordinary activity. Characteristics of these episodes and evidence for these findings are reviewed.     

Comparative study of exercise-induced ventricular arrhythmias in normal subjects and patients with documented coronary artery disease.

The incidence, types and patterns of emergence of treadmill exercise induced ventricular arrhythmias were studied in 482 subjects with and without coronary heart disease. All subjects were free of premature ventricular complexes at rest and were classified into groups on the basis of their clinical status. In Group 1A were 141 patients with chest pain and normal coronary arteriograms and in Group IB 144 age-matched subjects free of clinical evidence of heart disease. Group II consisted of 197 patients with chest pain and arteriographically documented coronary artery disease. Patients in Group IA and II exercised to at least 85% of their predicted maximal heart rate or until chest pain occurred. Subjects in Group IB underwent maximal exercise testing. The total incidence of exercise-induced ventricular arrhythmias was 16% in Group IA, 44% in Group IB and 29% in Group II. However, when exercise heart rate at the time of appearance of ventricular arrhythmias was taken into account the incidence of exercise-induced ventricular arrhythmias up to a heart rate of 130/min was 27% in the patients with documented coronary artery disease (Group II) compared with rates of 9 and 6%, respectively, for Groups IA and IB (P less than 0.001). The incidence rates of multifocal ventricular premature complexes, ventricular tachycardia and ventricular premature complexes at a rate of more than 10/min were also significantly greater at submaximal heart rates in the patients with coronary disease. Patients with three vessel coronary artery disease and abnormal left ventricular wall motion had a significantly greater incidence of exercise-induced ventricular arrhythmias. The incidence of exercise-induced ventricular arrhythmias in patients with coronary disease and a positive S-T segment response was not significantly increased.     

结节性多动脉炎合并心肌梗死8例临床分析

目的总结结节性多动脉炎累及冠状动脉导致心肌梗死患者的临床表现及冠状动脉受累特点。方法对北京协和医院有病案记录的结节性多动脉炎合并心肌梗死的8例患者的临床症状、系统受累、实验室检查、冠状动脉及其他血管造影、超声心动图和病理检查等进行回顾性分析。结果 8例患者中男性5例,女性3例,年龄21～52岁,平均(37.6±11.7)岁。胸痛6例,心力衰竭1例。心电图缺血性ST-T改变5例,除窦性心动过速、房性期前收缩外,未见其他恶性心律失常。左心室射血分数降低(≤50%)3例,节段性室壁运动异常6例,室壁瘤形成2例,心肌病变2例,肺高压1例。4例有冠状动脉影像学检查资料,均累及右冠状动脉,3例为三支病变,1例为两支病变,其造影结果描述为冠状动脉弥漫性病变、冠状动脉扩张、多发动脉瘤以及节段性狭窄、闭塞。这些患者均有其他多部位血管受累的表现和动脉造影检查的异常。结论结节性多动脉炎可累及冠状动脉导致心肌梗死,其冠状动脉受累常为多支病变、多有右冠状动脉受累,动脉瘤伴血栓形成和节段性狭窄。对冠心病低危心肌梗死的患者,需要完善血管检查,警惕结节性多动脉炎累及冠状动脉的情况。     

Clusters of life-threatening ventricular arrhythmias in patients with implanted cardioverter-defibrillators: prevalence, characteristics, and risk stratification

BACKGROUND: Series of discharges from an implanted defibrillator (ICD) to terminate life-threatening ventricular tachyarrhythmias are one particular aspect of energy use and success of ICD therapy. Little is known about prevalence. characteristics, and risk stratification of so-called "cluster arrhythmias." HYPOTHESIS: The objective of this study was to examine the frequency of cluster arrhythmias, to characterize the temporal relationship precisely, and to assess the accompanying circumstances of their occurrence, whereby risk stratification was to be made if appropriate. METHODS: In all, 63 consecutive patients were followed prospectively over 727 +/- 684 days to determine the presence and characteristics of cluster arrhythmias (45,801 patient days). In 30 patients, 374 ICD episodes of ventricular tachyarrhythmias were analyzed for their temporal relationship. After a first successfully terminated ventricular tachyarrhythmia, further ICD discharges within 3 h were observed during 145 of 374 (39%) episodes; mean time interval between these arrhythmias was 25 +/- 32 min. RESULTS: Arrhythmia clusters occurred in 19 of 30 (63%) patients. In multivariate analysis, only underlying heart disease was predictive for accumulation of ventricular tachyarrhythmias. Cluster arrhythmias were more frequent among patients with ischemic heart disease than among those with nonischemic heart disease (40.0 vs. 29.2%, p < 0.05). Ejection fraction, age, gender, and other parameters were not predictive for occurrence of arrhythmia clusters. In 4 of 19 patients, accumulation of ICD discharges was predictive for new onset of myocardial ischemia elicited by exercise test. CONCLUSIONS: Cluster arrhythmias are most common in patients with ICDs with coronary heart disease and may indicate disease progression and increasing instability, for example, due to new onset of myocardial ischemia.     

Ventricular Tachycardia in Coronary Artery Disease

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study.

OBJECTIVE: To evaluate the prevalence and prognostic significance of asymptomatic complex or frequent ventricular premature beats detected during ambulatory electrocardiographic (ECG) monitoring. DESIGN: Cohort study with a follow-up period of 4 to 6 years. SETTING: Population-based. PARTICIPANTS: Surviving patients of the original Framingham Heart Study cohort and offspring of original cohort members (2727 men and 3306 women). MEASUREMENTS: One-hour ambulatory electrocardiography. RESULTS: The age-adjusted prevalence of complex or frequent arrhythmia (more than 30 ventricular premature complexes per hour or multiform premature complexes, ventricular couplets, ventricular tachycardia, or R-on-T ventricular premature complexes) was 12% (95% Cl, 11% to 13%) in the 2425 men without clinically evident coronary heart disease and 33% (Cl, 24% to 42%) in the 302 men with coronary heart disease. The corresponding values in women (3064 without disease and 242 with disease) were 12% (Cl, 11% to 13%) and 26% (Cl, 9% to 43%). After adjusting for age and traditional risk factors for coronary heart disease in a Cox proportional hazards model, men without coronary heart disease who had complex or frequent ventricular arrhythmias were at increased risk for both all-cause mortality (relative risk, 2.30; Cl, 1.65 to 3.20) and the occurrence of myocardial infarction or death from coronary heart disease (relative risk, 2.12; Cl, 1.33 to 3.38). In men with coronary heart disease and in women with and without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk for either outcome. CONCLUSIONS: In men who do not have clinically apparent coronary heart disease, the incidental detection of ventricular arrhythmias is associated with a twofold increase in the risk for all-cause mortality and myocardial infarction or death due to coronary heart disease. The preventive and therapeutic implications of these findings await further investigation.     

Myocardial ischemia: current concepts and future perspectives

Ischemic heart disease is the leading cause of morbidity and mortality in a worldwide epidemic. Myocardial ischemia is characterized by an imbalance between myocardial oxygen supply and demand, causing cardiac dysfunction, arrhythmias, myocardial infarction, and sudden death. Various clinical ischemic manifestations are caused by obstruction of coronary blood flow by coronary plaques, thrombosis, and/or hyperconstriction/vasospasm of epicardial and microvascular coronary arteries, in which gender difference also is involved due in part to estrogen hormonal state. The coronary circulation matches blood flow with oxygen requirements by coordinating the resistances within microvasculature, where the endothelium plays an important role by liberating several vasodilator substances. The impaired endothelial regulation is involved in the pathogenesis of a wide variety of cardiovascular diseases and therefore is an important therapeutic target. Activation of Rho-kinase pathway is involved in the pathogenesis of both endothelial dysfunction and vascular smooth muscle hypercontraction and also should be an important therapeutic target.     

Hypertensive heart disease

Hypertensive heart disease encompasses anatomical changes and altered physiology of heart muscle, coronary arteries, and great vessels. Left ventricular hypertrophy is not only a target organ response to increased afterload, but is also the most potent cardiovascular risk factor. Regression of hypertrophy reduces morbidity and mortality. Heart failure may be present in the absence of a reduction of myocardial contractility. Ischemic heart disease occurs in the absence of epicardial coronary disease. Left atrial size and atrial fibrillation are associated. Potentially lethal ventricular arrhythmias and sudden cardiac death are more common in hypertensive patients. The relationship of aortic root size to blood pressure is weaker than expected; however, the relationship to aortic dissection is stronger. Careful attention and treatment of left ventricular hypertrophy, heart failure, ischemic heart disease, and atrial fibrillation will improve survival.     

Natural history and prognosis of ischemic heart disease

Forty-four cases with myocardial rupture (33 with free wall rupture, 9 with interventricular septal perforation and 2 with papillary muscle rupture), all of which were ascertained by autopsy and/or at surgery, were analyzed. When the following 7 risk factors were actively managed in the acute stage of myocardial infarction, the incidence of myocardial rupture was significantly reduced: a) high blood pressure on admission, b) physical and emotional instability, c) recurrent chest pain, d) aged females, e) no history of angina or myocardial infarction, f) large myocardial infarction on ECG and g) the first 10 days after the attack of myocardial infarction. If cardiogenic shock occurs, surgery should be performed as soon as possible; if not, it should be delayed 3 weeks. The natural history of ischemic heart disease was analyzed in 400 medically-treated patients with significant coronary artery disease. They had been followed up continuously and periodically for more than one year. The prognosis of the patients with 3-vessel disease or left main trunk disease, those with poor left ventricular function (EF less than 30%) and of old age (greater than or equal to 60) and those who had a history of ischemic heart disease was poor. Follow-up study was done in 30 patients with variant angina. They often had life-threatening arrhythmias during attacks (8 ventricular tachycardia or ventricular fibrillation, 8 serious bradyarrhythmia). All patients with variant angina should be treated medically at first, and only patients with organic coronary artery disease and chest pain on effort in spite of the medical treatment should be considered as candidates for AC bypass surgery.     

Taquicardia ventricular en la enfermedad coronaria

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Effects of major coronary artery stenosis on the pressure-flow relationship of an adjacent intact coronary artery branch in isolated supported canine left ventricle

We investigated whether the relationship between the mean left anterior descending and septal coronary blood flow and the mean perfusion pressure varies with left circumflex coronary stenosis. We used excised, perfused canine heart preparations (n = 10), in which variables to influence the myocardial oxygen demand and supply relation can be fairly well controlled. The results showed that coronary blood flow in the adjacent, non-stenosed coronary artery increased significantly following LCX stenosis; this increased flow was found at the same values of heart rate, left ventricular end-diastolic pressure and perfusion pressure, as those in the preischemic state. Moreover, this increased flow was also observed when the values of peak left ventricular pressure and pressure-length loop area were similar between the pre-ischemic and ischemic states. Thus, contributions of neurohumoral factors or alterations in mechanical factors determining the myocardial oxygen demand and supply relation are negligible. This increased flow may be important in maintaining overall cardiac function in cases of acute coronary stenosis or coronary occlusion.     

Standardized screening and treatment of patients with life-threatening arrhythmias: the Leiden out-of-hospital cardiac arrest evaluation study.

OBJECTIVES: The aim of this study was to evaluate the effect of a systematic screening/treatment protocol on outcome in patients after aborted sudden death. BACKGROUND: Patients after aborted sudden death are at high risk for recurrent events. In this regard, systematic screening is mandatory to reveal the underlying etiology, to detect and subsequently treat reversible causes, and to establish patient-tailored antiarrhythmic treatment. METHODS: A total of 417 consecutive patients after aborted sudden death due to ventricular arrhythmias underwent echocardiography and coronary angiography. In the presence of coronary artery disease and myocardial ischemia, using stress-rest myocardial perfusion imaging/exercise testing, subsequent revascularization was performed. Patients without ischemic heart disease were further evaluated with magnetic resonance imaging, contrast echocardiography, right ventricular angiography and/or flecainide/ergonovine testing. After these diagnostic steps, final antiarrhythmic therapy was based on the outcome of electrophysiologic testing. RESULTS: The majority of patients had ischemic heart disease (n = 300, 72%). After screening, 78 (78 of 300, 26%) patients underwent revascularization. In 69% of patients, ventricular arrhythmias were inducible during electrophysiologic testing. Therapy consisted of implantable defibrillators in 301 (72%) patients, antiarrhythmic drugs in 239 (57%) patients, and catheter ablation in 58 (14%) patients. During 5-year follow-up, only 3 (<1%) patients died suddenly. The 5-year survival rate was 82%; of 39 deaths, 10 (26%) patients died due to non-cardiac disease and 26 (67%) due to heart failure. CONCLUSIONS: Screening and treatment of patients after aborted sudden death according to a standardized protocol resulted in <1% arrhythmic deaths during 5-year follow-up. The majority of patients died of heart failure, stressing the importance of optimizing medical and surgical therapy and screening.