Thompson D S, Wilmshurst P, Juul S M, Waldron C B, Jenkins B S, Coltart D J, Webb-Peploe M M
Br Heart J. 1983 Mar;49(3):259-67. doi: 10.1136/hrt.49.3.259.
High fidelity measurements of left ventricular pressure were made at increasing pacing rates in 21 patients with hypertrophic cardiomyopathy and a control group of 11 patients investigated for chest pain who proved to have normal hearts. In both groups the fall in pressure during isovolumic relaxation from the point of min dp/dt approximated closely to a monoexponential, and could be described by a time constant and asymptote. The time constant shortened and the asymptote increased as heart rate rose in both groups. The time constant was longer and min dp/dt less in the cardiomyopathy group than controls at all heart rates. In the cardiomyopathy patients min dp/dt, but not the time constant, was related to systolic pressure. During pacing, eight cardiomyopathy patients developed metabolic evidence of myocardial ischaemia, but indices of relaxation did not differ between these eight and the other 13 either at basal heart rate or the highest pacing rate. In 10 cardiomyopathy patients measurements were repeated at comparable pacing rates after propranolol (0.2 mg/kg). Left ventricular end-diastolic pressure and indices of contractility decreased after the drug, but the time constant did not change. Eight patients received verapamil (20 mg) after which there were substantial reductions in systolic pressure and contractility. Min dp/dt decreased in proportion to systolic pressure, but the time constant was unchanged. At the highest pacing rate before drug administration three patients had abnormal lactate extraction which was corrected by either propranolol (one patient) or verapamil (two patients). Despite abolition of metabolic evidence of ischaemia, relaxation did not improve. It is concluded that abnormal isovolumic relaxation is common in patients with hypertrophic cardiomyopathy, but its severity correlates poorly with other features of the disease. Abnormal relaxation is not the result of ischaemia, and pressure derived indices of relaxation do not improve after the administration of propranolol or verapamil.
对21例肥厚型心肌病患者以及11例因胸痛接受检查且心脏正常的对照组患者,在逐渐增加起搏频率的情况下进行了左心室压力的高保真测量。在两组中,等容舒张期从最小dp/dt点开始的压力下降都非常接近单指数曲线,并且可以用一个时间常数和渐近线来描述。随着心率上升,两组的时间常数均缩短,渐近线均增大。在所有心率水平下,心肌病组的时间常数均长于对照组,最小dp/dt低于对照组。在心肌病患者中,最小dp/dt与收缩压相关,但时间常数与收缩压无关。起搏过程中,8例心肌病患者出现心肌缺血的代谢证据,但这8例患者与另外13例患者在基础心率或最高起搏频率时的舒张指标并无差异。对10例心肌病患者在服用普萘洛尔(0.2mg/kg)后以相当的起搏频率重复进行测量。用药后左心室舒张末期压力和收缩性指标下降,但时间常数未变。8例患者服用维拉帕米(20mg)后,收缩压和收缩性大幅降低。最小dp/dt与收缩压成比例下降,但时间常数不变。在给药前的最高起搏频率时,3例患者乳酸摄取异常,其中1例经普萘洛尔、2例经维拉帕米治疗后得到纠正。尽管缺血的代谢证据消失,但舒张功能并未改善。结论是,异常等容舒张在肥厚型心肌病患者中很常见,但其严重程度与疾病的其他特征相关性较差。异常舒张并非缺血所致,服用普萘洛尔或维拉帕米后,压力衍生的舒张指标并未改善。