Jurkovicova O, Cagan S
IV. interna klinika Lekarskej fakulty Univerzity Komenskeho v Bratislave, Slovakia.
Bratisl Lek Listy. 1998 Mar;99(3-4):172-80.
In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI, SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: Ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinically course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure cardiogenic shock and malignant ventricular arrthythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.).
除室性心律失常外,各种形式的室上性心律失常(SVA)以及房室(AV)和室内(IV)传导障碍在急性心肌梗死(AMI)中也会出现。在AMI情况下,SVA可能由相关的心房缺血或梗死引起。SVA会使病程复杂化,尤其是下壁、后壁和侧壁AMI,在右心室心肌梗死和心包炎中SVA也经常出现。AMI后期出现的SVA尤其由血流动力学因素引起,特别是左右心室功能障碍的因素。心房扩张和心房内压力升高也是SVA发生的重要因素。自主神经系统、电解质紊乱、酸中毒和全身性缺氧可能作为SVA发生发展的调节因素。下壁AMI患者的房室传导障碍明显比前壁AMI患者更常见。在下壁AMI中,它们常由反射性副交感神经激活引起。在房室传导障碍的发生过程中,以下机制也可能起重要作用:房室结或房室交界区的缺血或坏死以及心肌缺血和再灌注期间大量释放的腺苷和钾的负性变传导作用。下壁AMI病程中并发的高度房室传导阻滞预后明显好于前壁AMI时出现的高度房室传导阻滞。在下壁AMI中,房室传导阻滞通常是可逆的,而在前壁AMI中,它是持续性和不可逆的。AMI后24小时内出现的早期房室传导障碍预后优于AMI后期出现的房室传导障碍。AMI病程中并发的束支传导阻滞(BBB)是由与束支相关的冠状动脉闭塞或其供血区严重缺血引起的。BBB通常是多支血管病变的标志。AMI中出现的新的BBB,尤其是右束支传导阻滞被认为是完全性房室传导阻滞发生的预测指标。频繁和反复出现的SVA以及严重的房室和室内传导障碍常与AMI明显更差的临床病程和死亡率增加相关,尤其是医院死亡率增加。然而,这通常不是由SVA或房室和室内传导障碍本身引起的。这些患者的主要死亡原因是心力衰竭、心源性休克以及由于大面积AMI、左心室功能显著降低和晚期冠心病导致的恶性室性心律失常。复杂的SVA以及严重的房室和室内传导障碍通常被视为标志,但不是医院死亡率增加以及在某些情况下院后死亡率增加的独立预测指标。它们在AMI中的出现可能有助于识别需要强化治疗(包括积极处理广泛冠心病)的高危患者。(参考文献62.)