Medical Research Society
clinic.
n
mycm
118
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68.7p.7) 67.8v.1)
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69.3p.3)
53
71.3(9.1)
0.12.
M9 ENDOTHELIAL. DYSFUNCTION IS NOT THE
LIMITING FACTOR IN SKELETAL MUSCLE FUNCTION
OF PATIENTS WITH CHRONIC HEART FAILURE
AK NIGHTINGALE^, JG CRILLEY*. NC PEGGE, M SCHMTT,
R FIELD, C MUMFORD and MP FRENNEAUX'C inhoduced by*)
Department of Cardiology, Wales Heart Research Institute,
University of Wales College of Medicine, Cardiff CF14 4XN, UK
*Magnetic Resonance Unit, John Radcliffe Hospital, Oxford
I
w-
WrmM
31%
I
24%
II
33%
34%
0.54.
rrullh
Maading
* p=<0.05 compared to Caucasians, * -0.05
comparedto Al r
Caribbeans, ~ 9 %
one way ANOVA.
Results: Indo-Aslansand Afrocanbbeans were srgrufidy less aware
of AF as a heart ccnrhmn and coase~uencesof AF canpared to
Caucasians More Mo-Aslans were obhvlous to the beneficial efFect of
Warfarin and the reasons for takmg the tablets Only 31% of the whole
pahentgroup was awareofthe blnsks ofwarfann
Conclusion: Knowledge of AF as a d~seaseand the benefitdnsks of
warfann therapy was sub opbmal amongst pahents wltb AF In parhcular,
Indo-Asmn and Afrc-Canbbeans had the least awareness With mreasmg
p r e v a b x of AF and greater stress on anhcoagulahon, pahent educahon,
mcreased awareness and particrpahoo m their maDaganent rerrrmtls vltal
M8 HIGH ENERGY DC CARDIOVERSIONFOR
ATRIAL FIBRILLATION GAIN WITHOUT PAIN?
C BOOS, G WILBOURNE,M THOMAS and R MORE
Background: Chronic heart failure (CHF) is a condition
characterised by marked exercise intolerance. Non-invasive studies
using "P magnetic resonance spectroscopy ("P MRS) have shown
that patients with CHF have prolonged recovery half times for high
energy phosphates (PCr tM). Vitamin C (VC)has been shown to
improve endothelial function in conduit and resistance vessels. We
therefore hypothesised that chronic oral VC might improve skeletal
muscle blood flow and thereby improve exercise capacity and
muscle energetics in patients with CHF.
Merhods: 22 CHF patients (NYHA class II or m) were studied. We
assessed six minute walk distance, skeletal muscle energetics (3'P
MRS), pulse wave velocity (PWV) at baseline and response to
reactive hyperaemia (RH) in the leg. Subjects received VC (4glday)
or placebo (P) for a month and were then restudied.
Results:Data are expressed as mean f SEM.
I P baseline I P.f _
i
IVCbase IVC6
_ . 1
6minwalk(m) 3OOi24
3-6
If15
4Of24
PCr tH (sec)
6639
0.5f10
61f12
0.71t7
PWV(rn/~ec)
9.9M.6
O.M.7
9.3M.9
-0.4M.5
PWVRH(%)
6.lf2.9
6.3326;
13.1M.5
-5.033.4
*p<0.05compared to placebo. All other comparisons were NS.
Conclusion: Although there was no improvement in basal PWV
following VC, the response to reactive hyperaemia did improve
suggesting an improvement in large artery endothelial function.
Despite this, there was no increase in exercise capacity nor
improvement in muscle energetics, suggesting that endothelial
dysfunction is not the limiting factor in muscle function in CHF.
Dept of Cardiology, St. Mary's Hospital, Milton Rd,
Portsmouth, PO3 6AD
Background: Directcurrent cardioversion (DCCV) remains an
effective treatment for the restoration of sinus rhythm in patients in
atrial fibrillation (AF). However the optimal energy level settings
have not been fully evaluated in a large series of contemporary
patients.
Methods: A cohort of 84 patients in persistent atrial fibrillation
(AF) was prospectively randomized to an initial synchronized
DCCV shock of 360 joules (J) versus UWlJ. The shock sequence
thereafter of 4 further shocks was similar for the 2 groups: 1 X
3601 anterior-anterior(AA), 1 X 360J AA, 1 X 36OJ anteriorposterior (AP)and 1 X 36OJ AP. In a subgroup of 53 patients (25
vs 28 patients), the levels of creatine kinase (CK) and aspartate
transaminase (AST)were measured the following day post
cardioversion. In this subgroup we also measured the change in
cardiac troponin I (cTnI) with each DCCV.
Results:The success rate for DCCV was significantly higher in
the 360J gro,up compared to the UWlJ group (29/31= 93.54%vs
39/53 = 73.58%,pd.04). The average peak CK (1212.6 vs 2330.1,
~4.068)and AST (38.8 vs 79.33, pS.098) were non-significantly
lower in the 360J group than in the UWlJ group. There was no rise
in cTnI in either group. The average number of shocks (1.84 vs
2.64, pd.008) was significantly less in the 360J group than in the
UWlJ group, with a trend to lower total energy requirements for
DCCV in tHe 360J group (661.9J vs 797.8J. pd.215).
Conclusion: For patients in persistent AF the use of a higher initial
energy shock of 360J at DC cardioversion achieves a significantly
greater success rate, with less skeletal muscle damage (with no
cardiac muscle damage) as compared with a Lower energy DC
shock.
M I 0 EFFECT OF VITAMIN C ON VENTRICULAR
VASCULAR COUPLING IN PATIENTS WITH CHF
AK NIGHTINGALE*, M S C H M m , NC PEGGE, R FIELD,C
MUMFORD and MP FRENNEAUX'
(*introduced by?
Department of Cardiology, Wales Heart Research Institute,
University of Wales College of Medicine, Cardiff CF14 4XN, UK
Background: Chronic heart failure (CHF) is characterised both by
left ventricular systolic dysfunction and increased vascular tone. The
latter results in increased pulse wave velocity with early return of
reflected waves. contributing to reduced left ventricular systolic
ejection duration (ED). We have previously shown that acute
intravenous administration of vitamin C (VC) delays wave reflection
and therefore investigated whether a similar response could be
achieved with chronic oral VC therapy.
Methods: 22 CHF patients (NYHA class II or m) were studied.
After 20 minutes supine rest pulse wave analysis was performed.
This technique relies on the principal of aplanation tonometry and
records a radial pulse contour from which the integrated software
(SphygmoCor version 6.2, PWV Medical) derives a central aortic
waveform via a validated transfer function. From this, ED can be
calculated. Subjects were randomised to oral VC 4g daily or placebo
(P) for one month in a double blind parallel group study and
measurements were repeated.
Results: Data are expressed as mean f SEM. The groups were well
matched for age and sex. BP was similar in both groups (systolic
BP; VC 129i8 mmHg v P 1 3 2 8 mmHg: P = NS) as was heart rate