Fifty-one patients (mean age 51.6 +/- 7.1 years) with angiographically proven coronary artery disease (CAD) entered the study. In 26 patients (Group I), trimetazidine treatment started twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA). Another 25 patients (Group II) without trimetazidine treatment were kept as controls. The groups were comparable by age, gender, risk factors of CAD, coronary anatomy, left ventricular performance, and heart rate variability indices at baseline state. Power spectral analysis of heart rate variability and two-dimensional and Doppler echocardiographic examinations were performed before PTCA, and twenty-four hours, ten days, thirty days, and three months after PTCA. A statistically significant improvement of left ventricular systolic performance (P < 0.001), augmentation of the parasympathetic band of heart rate variability (P < 0.001), and decline of P1/P2 ratio (P < 0.01) were evident in patients treated with trimetazidine, while no apparent changes were observed in controls. The intergroup analysis also showed marked difference between groups as recorded on the day 30 and month 3 of observation (P < 0.001). During follow-up period recurrences of angina pectoris and ischemia were registered in Group II, while no evidence of ischemia was discerned in Group I patients. In conclusion, trimetazidine modulates the autonomic control of heart rate, ie, reduces sympathetic overactivity and augments vagal influences, improves left ventricular contractility, and diminishes the clinical manifestations of ischemia in patients with CAD after PTCA.

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Although experimental studies have demonstrated that reduced glutathione (GSH) is involved in cellular protection from deleterious effects of oxygen free radicals (OFRs) in ischemia and reperfusion, there are controversial data on the correlation between the levels of erythrocyte GSH and the ischemic process. To clarify, we determined the erythrocyte GSH levels in 21 patients with acute myocardial infarction (AMI), aged 39-70, who were not given thrombolytic therapy and 21 age-and sex-matched healthy controls. Samples of blood were taken on days 1, 3, 5 and 7 from AMI patients and on the same days from the controls.

Transient and rapidly recovered, especially parasympathetically modulated HRV reduction occurred after PTCA in patients with single-vessel disease. HRV reduction is associated with PTCA restenosis risk score and the degree of revascularization as invasive feature of angioplasty, hence it may be related to reperfusion.

We read with interest the articles of Rama et al. [ 1 J and Kinn et al. [2] concerning cortical blindness after cardiac angiography .They found transient cortical blindness (TCB) after cardiac catheterization secondary to a rare complication of contrast usage. TCB is characterized by complete loss of visual perception and optokinetic nystagmus with preservation of ocular motility, pupillary responses, and normal fundoscopic examination [3]. It results from bilateral cerebral lesions, posterior to the lateral geniculate bodies affecting either optic radiation as occipital cortex.It has been suggested that its occurrence is due to an adverse reaction to radiographic contrast agent-induced cerebral toxicity. Incidence of TCB has been reported to be 0.3-4% with cerebral and vertebral angiography [4,5]. It has also been reported with myelography , brachial angiography , and aortography . TCB after coronary angiography is exceedingly rare. The incidence of it after diagnostic catheterization is 0.05% in Kinn's series [2].Contrast induced TCB occurs within minutes to 12 hours after angiography. The occipital cortex is more vulnerable to contrast material because the blood brain barrier over the visual cortex is reportedly incomplete, thereby permitting selectively increased access of contrast material to the visual cortex [4].The precise mechanism of toxic effect by contrast material is speculative, but may be due to direct effect, idiosyncratic reaction, microembolism, hypoxia, or edema. TCB usually resolves completely within 2 to 7 days [I]. No therapy has proven effective in accelerating the resolution of TCB. The occurrence of blindness and the timing were unrelated to the amount and osmolality of contrast received [6]. Rama et al. found that reexposure to contrast during subsequent cardiac catheterization did not develop TCB in their three cases, which had developed TCB following first exposure to contrast. They used the same type of contrast (Optiray 320, nonionic by Mallinckrodt) during each cardiac catheterization.We present a 55-year-old white male patient with unstable angina pectoris, who developed TCB following second exposure to contrast during a second diagnostic coronary angiogram. During the first diagnostic coronary angiography , TCB had not developed, but about 3 months later, the second diagnostic coronary angiogram was performed, because of unstable angina pectoris, with the same contrast (iopromid 320) and approximately the same amount (total used 120 ml at first procedure, 130 ml at second procedure). TCB developed about 6 hours later and resolved incompletely within 7 days, completely within about 3 weeks without taking any drug. Our patient did not demonstrate any neurological abnormality on the CT scan of the head or on the electroencephalogram. We believe that it was not hysterical blindness. Embolism, vascular spasm, or thrombotic events causing amourosis fugax or homonymous hemianopsia were excluded. The patient did not have arthralgias or purpura, etc.This event in our patient may lead to ...