Kass D A
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287, USA.
Basic Res Cardiol. 1998;93 Suppl 1:108-16. doi: 10.1007/s003950050232.
Our study demonstrated a loss of normal systolic contractile enhancement with increasing heart rate in patients with ventricular hypertrophy and symptoms of congestive heart failure. This decline in systolic reserve was not accompanied by worsening of diastolic function, and would therefore not seem to reflect underlying ischemia. Rather, it was more likely related to abnormalities of excitation-contraction coupling, particularly in light of findings of both increased post-rest potentiation and a reduced recirculation fraction. In contrast, mechanical restitution was unchanged, suggesting that alterations in Ca2+ release from the SR did not play a major role. Finally, we showed that increasing heart rate adversely affects the efficiency of ventriculo-vascular coupling in LVH hearts. This suggested another explanation of how dysfunction of cardiac force-frequency behavior can lead to limited cardiovascular reserve and contribute to clinical symptoms of exertional intolerance. Future efforts aimed at enhancing the force-frequency response, perhaps by enhancing the SR-ATPase, or manipulating its regulation, should prove helpful in ameliorating the limitations of LVH patients associated with rapid heart rate.
我们的研究表明，在患有心室肥厚和充血性心力衰竭症状的患者中，随着心率增加，正常的收缩期收缩增强功能丧失。收缩储备的这种下降并未伴有舒张功能恶化，因此似乎并不反映潜在的缺血情况。相反，它更可能与兴奋 - 收缩偶联异常有关，特别是考虑到静息后增强增加和再循环分数降低的发现。相比之下，机械恢复不变，表明肌浆网Ca2+释放的改变未起主要作用。最后，我们表明心率增加对左心室肥厚心脏的心室 - 血管耦联效率产生不利影响。这提示了另一种解释，即心力 - 频率行为功能障碍如何导致有限的心血管储备并促成运动不耐受的临床症状。未来旨在增强力 - 频率反应的努力，或许通过增强肌浆网ATP酶或操纵其调节，应有助于改善左心室肥厚患者与快速心率相关的局限性。
