P. Gramlingbabb et al., TREATMENT OF MEDICALLY AND SURGICALLY REFRACTORY ANGINA-PECTORIS WITHHIGH THORACIC EPIDURAL ANALGESIA - INITIAL CLINICAL-EXPERIENCE, The American heart journal, 133(6), 1997, pp. 648-655
Surgical sympathectomy can relieve symptoms of angina in patients with
refractory angina. However, in these high-risk patients this thoracic
surgery may result in significant morbidity and mortality rates. Simi
lar sympathetic blockade can now be produced with high thoracic epidur
al analgesia (HTEA). From September 1995 to August 1996, we treated 10
consecutive patients with HTEA. These eight men and two women, aged 5
8 +/- 5 years, with extensive three-vessel coronary disease and ejecti
on fractions of 40% +/- 5%, had New York Heart Association (NYHA) clas
s IV angina despite medical therapy, including nitrates, beta-blockade
, calcium channel blockade, and narcotics. HTEA was performed at the T
1 through T4 levels with a catheter placed either percutaneously or su
rgically, with radiographic confirmation of catheter placement with an
epidurogram or computed tomography scan. Bupivacaine (0.25% to 0.5%),
an amide local anesthetic, was given as a bolus through the epidural
catheter and then maintained either as a continuous infusion or an int
ermittent rebolus. The epidural catheter remained in place for 7 days
in four patients, 14 days in three patients, and greater than or equal
to 90 days in three patients. Before consideration for HTEA, each pat
ient was deemed unsuitable for or refused coronary bypass surgery and
percutaneous coronary angioplasty and had NYHA class IV symptoms of an
gina. Seven of 10 patients required intravenous nitroglycerin and hepa
rin and were unable to be discharged from the intensive care unit beca
use of anginal symptoms. Two of these seven patients also required an
intraaortic balloon pump for symptom control. After HTEA, all 10 patie
nts had improved symptoms, with five patients improving to NYHA class
II symptoms and five improving to NYHA class III. All seven patients r
eceiving intravenous nitroglycerin, heparin, or intraaortic balloon pu
mp support had these modalities discontinued. Six of these seven patie
nts were subsequently discharged from the hospital. One patient died f
rom a non-HTEA related cause. There were no HTEA-related deaths. There
were three catheter-related complications necessitating catheter remo
val during 12 months of HTEA use. Local infection developed in one pat
ient, one had catheter occlusion caused by fibrosis, and one patient h
ad chronic back pain exacerbation from a paraspinous muscle spasm. No
patient had a myocardial infarction or a significant arrhythmia. In pa
tients with otherwise intractable angina pectoris, HTEA is an effectiv
e modality that produces symptomatic relief of angina pectoris and all
ows increased activity level.