Læknablaðið - 15.12.1986, Page 71

LÆKNABLAÐIÐ
371
þennan sjúkdóm, 76 karlar og 56 konur. Meðalaldur við
greiningu er rúm 69 ár hjá báðum kynjum. Árin
1971-1975 greindust 35 með sjúkdóminn, á næstu fimm
árum 43 og 1981-1985 voru 52 sjúklingar greindir. Fimm
ára lifun (survival) er 14,3% hjá þeim sem greindust á
tímabilinu 1971-1975 en 16,3% næstu Fimm á á eftir.
Tíu ára lifun á tímabilinu 1971-1975 er 2,9% (eitt
tilfelli).
Niðurstöður benda til þess að nýgengi sjúkdómsins sé
hærra hérlendis en víðast hvar og fari vaxandi.
ACE INHIBITORS IN HEART FAILURE
H. J. Dargie. Western Infirmary, Glasgow.
An array of neuroendocrine responses results from and
indeed may aggravate the fall in cardiac output and
increase peripheral vascular resistance that is found in
most patients with chronic congestive heart failure
secondary to left ventricular dysfunction. This
biochemical spectrum includes increased plasma
concentrations of renin angiotensin II (AII),
aldosterone (ALDO), arginine vasopressin (AVP) and
noradrenaline (NA). Appropriate in haemorrhage or
dehydration, these responses are not wholly beneficial in
cardiac disease and, in concert with what has aptly been
described as »unintelligent behaviour of the kidneys«,
may be responsible for the salt and water retention that
completes the clinical syndrome of raised venous
pressure and oedema or »heart failure« in patients with
severely compromised left ventricular function.
ACE inhibitors reduce the plasma concentrations of
AII, ALDO, AVP and NA and acutely this is
accompanied by fall in systemic vascular resistance that
correlated with pretreatment levels of renin. The full
haemodynamic profile includes reduction in arteriolar
and venous tone, right and left atrial, pulmonary and
systemic arterial pressures, together with little change or
slight fall in heart rate and a modest increase in cardiac
output. Qualitatively these effects are maintained in the
long term though their magnitute is less and serveral
double-blind placebo-controlled clinical trial have
demonstrated that they are accompanied by an
improvement in tirednesss and breathlessness, an
increase in exercise capacity and a decrease in
ventricular dimensions and arrhythmias. Interestingly
these long term benefits seem less closely related to the
pretreatment renin with the exception of the correction
of hypokalaemia and depleted total body potassium.
Potential problems include initial hypotension that can
be severe and life-treatening, renal dysfunction,
hyperkalaemia, hyponatremia, cough and angioneurotic
oedema. Other toxic effects including skin rash and
dysgeusia and their relationship to the sulphhydro
chemical grouping remain the subject of debate. The
most common mode of demise in heart failure
secondary to left ventricular dysfunction is sudden
death due to presumed ventricular arrhythmia and
preliminary data from our own prospective follow-up
series suggests that treatment with ACE inhibitors may
be beneficial in this respect also. Acute myocardial
infarction is accompanied by a similar neuroendocrine
response especially in patients with left ventricular
failure.
The raised level of AII, AVP and nonadrenaline could
have important implications for myocardial perfusion
and cardiac function: and experimentally Captopril
reduced infarct size. Titration of low doses of Captopril
in acute myocardial infarction produces a
haemodynamic profile similar to chronic heart failure
and may be worth exploring especially in patients with
left ventricular failure after myocardial infarction.
LEFT BUNDLE-BRANCH BLOCK, PREVALENCE,
INCIDENCE, FOLLOW-UP
ECHOCARDIOGRAPHY AND EXERCISE
TESTING
Guómundur J. Elíasson, Kjartan Pálsson, Kristján
Eyjólfsson, Atli Árnason, Þórður Haróarson, Nikulás
Sigfússon. Lyflækningadeild Landspítalans,
Hjartavernd.
In a randomly selected population screening study of
8450 men aged 33 to 61 and 9.000 women aged 34 to 61
conducted in Iceland in 1967-1977, 27 men and 17
women were found to have left bundle branch block
(LBBB). By 1977, the prevalence was 0.43% in men
(mean age with LBBB 58.9) and 0.28% in women (mean
age 58.5). The annual incidence of LBBB was 3.2.104 in
men and 3.7.104 in women. All 36 alive patients with
LBBB were examined in 1984 including chest x-ray,
echocardiography and exercise testing (Bruce protocol).
Eight men and no woman had had a myocardial
infarction (p<0.05), 9 men and 3 women had angina
pectoris, 10 women and 5 men had hypertension
(p<0.02), 5 men had cardiomyopathy, 7 men and 6
women had primary conductive disease, 2 patients had
pacemakers. Eleven patients were asymtomatic, 11 had
mild and 14 severe functional limitations. Five men and
two women had died in comparison with 18 men and 1
woman in an age-matched control group of 176 people
(p:n.s.). Three of 5 deceased LBBB men had
cardiomyopathy at autopsy. Three men died suddenly.
The two women died of noncardiac causes. Only one
patient in the control group had cardiomyopathy
(p<0.01). There was no significant difference in other
cardiac diagnosis between the groups. Eleven LBBB
women out of 13 had normal exercise duration (6 min)
and 11/17 men exercised normally (7 min). Nine men
and two women had an increased LV diameter and 3
men and 2 women had septum thickness > 1.5 cm by
echocardiography. In comparison with the control
group, the LBBB patients had an increased LV diameter
2.85 ±0.38 vs 2.58±0.38 cm/m2 body surface area
(p < 0.01) and non-significant increase in
intraventricular septum thickness. There was no
difference between the groups in left atrial diameter.
In conclusion, cardiomyopathy in men and
hypertension in women are associated with LBBB. The
prognosis of LBBB is good and few patients require
pacemakers. The LV diameter is increased in randomly
selected patients with LBBB.
HJARTAGANGRÁÐAR Á LANDSPÍTALANUM
1968-1985
Bjarni Valtýsson, Árni Kristinsson. Lyflækningadeild
Landspítalans.
Rannsókn þessi fjallar um 199 einstaklinga, 76 konur og
123 karla, sem fengu hjartagangráð á Landspítalanum á