No abstract

No abstract

No abstract

Cardiac arrhythmias are noted in a significant proportion of chronic renal failure (CRF) patients on hemodialysis (HD), and may contribute to cardiovascular mortality. A number of factors have been implicated in the genesis of these arrhythmias. The role of silent myocardial ischemia (SMI), however, has not been evaluated systematically. We prospectively studied 38 unselected CRF patients on regular HD by continuous Holter monitoring starting 24 hours before HD, lasting through the dialysis session and continued for 20 hours thereafter. The recordings were analyzed for frequency, timing and severity of supraventricular and ventricular arrhythmias and SMI as identified by ST-segment depression. Ventricular arrhythmias during HD were noted in 11 (29%) patients (group I), and were potentially life-threatening (Lown Class III and IVa) in 13%. The remaining 27 patients (group II) had no ventricular arrhythmias during HD. There was no difference in the age, sex ratio, duration of HD, blood pressure, fluctuations in weight, hematocrit, predialysis creatinine, sodium, potassium, calcium or inorganic phosphate levels between patients in the two groups. The number of patients with clinical ischemic heart disease was significantly greater in group I. SMI was noted in 72% and 33% of group I and II patients respectively (p = 0.026). 46% of those with and 25% of those without ST changes during HD developed ventricular arrhythmias during HD. Both SMI and ventricular arrhythmias were noted most frequently during the last hour of dialysis. Hypertension, diabetes mellitus and ischemic heart disease were observed more frequently amongst patients with SMI. Ventricular arrhythmias are detected in a significant proportion of CRF patients on HD. These are probably related to coronary artery disease since silent myocardial ischemia is also noted more frequently during HD in these patients. Further studies incorporating coronary angiography are needed in a larger number of patients to establish a definite causal relationship.

No abstract

The occurrence of silent myocardial ischemia (SMI) and serious arrhythmias during hemodialysis (HD) has been well documented. However, it is unclear whether these changes are due to epicardial coronary artery disease (CAD). We conducted a prospective study to assess whether SMI and arrhythmias during HD correlated with angiographically demonstrable CAD. Twenty-three patients with end-stage renal disease on maintenance HD underwent 48-hour Holter monitoring, beginning 24 hours prior to a HD session. All patients underwent biochemical evaluation, coronary angiography, and echocardiography. Holter monitoring showed SMI during HD in 22% cases. A significant increase in the frequency of ventricular ectopics (VEs) was noted during and after HD. Patients who showed SMI during HD and VEs prior to initiation of dialysis were more likely to develop significant ventricular arrhythmias during and after HD. Epicardial CAD was documented in four patients, and it did not correlate with SMI. To conclude, HD is an arrhythmogenic process. SMI during dialysis is probably not due to epicardial CAD but predisposes to clinically significant ventricular arrhythmias during and after HD. The cause of SMI during HD in patients without demonstrable CAD needs further investigation.

The occurrence of silent myocardial ischemia (SMI) and serious arrhythmias during hemodialysis (HD) has been well documented. However, it is unclear whether these changes are due to epicardial coronary artery disease (CAD). We conducted a prospective study to assess whether SMI and arrhythmias during HD correlated with angiographically demonstrable CAD. Twenty-three patients with end-stage renal disease on maintenance HD underwent 48-hour Holter monitoring, beginning 24 hours prior to a HD session. All patients underwent biochemical evaluation, coronary angiography, and echocardiography. Holter monitoring showed SMI during HD in 22% cases. A significant increase in the frequency of ventricular ectopics (VEs) was noted during and after HD. Patients who showed SMI during HD and VEs prior to initiation of dialysis were more likely to develop significant ventricular arrhythmias during and after HD. Epicardial CAD was documented in four patients, and it did not correlate with SMI. To conclude, HD is an arrhythmogenic process. SMI during dialysis is probably not due to epicardial CAD but predisposes to clinically significant ventricular arrhythmias during and after HD. The cause of SMI during HD in patients without demonstrable CAD needs further investigation.

No abstract