ABSTRACTS
THE ROLE OF ALDOSTERONE AND ALDOSTERONE ANTAGONISTS IN CONGESTIVE HEART FAILURE IN INFANCY Barry Baylen MD, Greqory Johnson MD, Reqinald Tsana MBBS. Laxm; Srivastava PhD; Simuel Kaplan MD,-FACC, Univ: of Cincinnati. Cincinnati. Ohio The failure of infant; with severe congestive heart failure (CHF) and congenital heart disease (CHD) to respond to conventional diuretic therapy is a conrmon indication for surgical intervention. Secondary hyperaldosteronism may be a major complicating factor in these patients and may contribute to their lack of response to medical therapy. We measured serum aldosterone (ald) by radioimnunoassay (micro-technique) in 8 infants (age 4 days-9 mos) with CHF secondary to CHD and in 20 normal control infants. Mean ald of controls was 23 ng%, range 2.8-75.5, which is similar to normal values previously described. In contrast, ald was markedly increased ,(y;r;;;)in 6 of 8 infants with CHF (mean=322.5 ns%, range . Several patterns of response to digoxin and intramuscular furosemide were observed in our patients. The 2 infants with normal ald responded well as manifested by clinical improvement, increased urinary output and increased urinary Na to K ratio (Una/Uk). By contrast, in 5 of 6 patients with increased ald, response was poor as reflected by decreased post-furosemide urinarv outout and reversed Una/Uk in the bresence of clinical signs of-p&-sistent fluid retention and normal or low serum osmolalitv. The addition of an aldosterone antagonist to the medical reqimen of 4 of these oatients resulted in markedlv improved post-furosemibe diuresis and increa&d Una/Uk. As signs of CHF cleared, ald fell siqnificantlv (~c.01). Hyperaldosteronism can be easily recognized by-eialuat;on of clinical course and serum and urine electrolytes and osmolalities and can be confirmed by serum ald assay. The recognition and treatment of hyperaldosteronism is important for optimal medical management of these infants.
CONDITIONS FOR "CORONARY STEAL" WITH DIPYRIDAMOLE. Lewis C. Becker,MD,FACC.Johns Hopkins Hosoitol.&Iltimore. MD Coronary vosodilot& have-been advbcated fo; red&on of a&e myocardial infarctionsize.Dipyridomole,o potent coronary orteriolar dilator, increasesflow to &chemic myodardium after cbronary ligation in the dog when the other coronarv arteries are normal _ However, the situ&ion might be morkedlybifferent when stenoies are present in the other orteries.Accordingly, in 10 anesthetized dogs, the distal left anterior descending (LAD) artery, was ligated and screw occluders olaced on the oro$mal LAD and circumflex (LC) arteries to reduce peak reoctiv’e hyperemio b 38 to 67%; resting flow remained normal .Regionol myocordia r flow was measured with 8-10~ diameter rabiwctiv& microspheres 1 hour after I igation, before and after l-1.5 mg/kg dipyridamole IV;myocardial injury was estimated by ST elevation in epicardial ECG’s.Heart rate was maintained constant by atria1 pacing and blood pressure (BP) by methoxomine infusion.Despite constant BP, dipyridamole caused a decrease in mean flow in ischemic myocordium from .22+ .02 to .l&.Ol ml/min/g (SEM,p<.Ol) while mean ST segment elevation Zcreased from 30.4+4.9 to 58.0t7.4mV (p c.05). In non-ischemic myocardium flowincreased from 1 .20 to 1 .61 ml/ min/g,but a marked maldistribution between inner (I) and outer (0) wall appeared (l/O; 1 .OOt.O2 to 0.30+.06,p<.OOl). In a second group of 6 dogs given dipyridamole, inflow restriction by the screw occluders wos less severe.ln this group in contrast to the first,Flow to ischemic muscle increased (. 14 to .I9 ml/min/g) and ST elevotion declined (55.6+21.2 to 41.0+35..5, ~~0.05). Thus, a “corona~steal” (reducfion in collateral flow at constant BP) is seen after dipyridamole only when the coronary arteries supplying collateral vessels are significantly stenosed.ln this setting dipyridamole causes reduced collateral flow and increased ST elevation.When stenoses are absent, dipyridomole appears to improve collateral flow and lessen the extent of myocardial injury.Therefore, whether coronary dilators ore beneficial or detrimental after acute coronary ligation is dependent upon the degree of obstruction of other coronary vessels.
120
January 1976
The American Journal of CARDIOLOGY
CORONARY ARTERY DILATATIONS. THEIR INFLUENCE ON LEFT VENTRICULAR FUNCTION AND PROGNOSIS. Benjamin Befeler, MD, F.A.C.C., Juan !I. Aranda, "ID, Nabil El-Sherif, MD and Ralph Lazzara, MD. VAH/University of Miami School of Medicine, Miami, Florida. Fourteen adult male patients evaluated angiographically because of symptoms of ischemic heart disease, either angina pectoris (AP) or congestive heart failure (CHF) exhibited fusiform or saccular coronary arterv dilatations (CAD)or aneurysms. Analysis of seqmental and overall left ventricular function disclosed that all patients had left ventricular dysfunction (LVD), manifested bv either decreased ejection fraction or decreased segmental motion, regardless of the degree of coronary obstructive lesions (COL), which accompanied a given dilatation. Eight patients exhibited AP, five CHF and one both. Four were class II, 8 class III and 2 class IV. Nine patients had diffuse dilatations, 3 had saccular and 2 both. In 10, the right coronary artery was involved, in 7 the circumflex and in 3 the anterior descending. Nine patients underwent surgery, LV aneurysmectomy or aorta-coronary bypass or both. Three patients had no COL but exhibited segmental LVD corresponding to the area of CAD. LVD can be related to CDL or CAD. AP was present in patients with and without COL. The patients were followed from 6 to 48 months (average 28). Twelve are alive today. One died of GI bleedinq with similar lesions in the mesenteric artery system. Adult patients demonstrating CAD form a subset cf individuals with ischemic heart disease, with a course more benign than common obstructive coronary arteriosclerosis. CAD are capable of producing AP and segmental LVD with and without COL.
IDIOPATHIC
PROLAPSE
137 PATIENTS
IN
Jorge
Belardi,
William
C.
Clinic One
hundred
abnormalities
could
be
disease
18-75
years
performed
(2
of
cally
One
of
of
pts.
cardiac
icant
II0
MR
the
110
causes: at
the
failure
secondary
cardiac
causes
complications
a
or 2
time
of
to
occurred
requiring
permanent
atrial
The
majority
course. is
a
Volume 37
heart had
died
of
pts.
died
rhythm.
pts.
died
signif-
congestive of
hip).
non-
Nonfatal
subacute
2 developed
atrial
bacterial
endocarditis
fibrillation. of of
small
treated
for
of
fractured
18% medi-
8 pts.: 2 developed subacute 3 developed complete AV block
pacemakers, I had
pts.
Significant
incidence
the
treated
(neither 3
age
in
endocarditis,
and
at
Five
and
in
was
MR.
Three
valve coro-
regurgitation
except
significant
stroke,
ranged
were
course
MR.
or
mortality
pts.
were
mitral
observed
disturbances
study),
angiograph-
replacement
mitral
day
suddenly
severe
(cancer,
and
30
pts. valve
were
benign minor
died
bacterial fibrillation
The
severe
The
had
MD;
Cleveland
(MVP)
rheumatic
Mitral
for
with
in whom
to
tendineae
had
STUDY
Manubens, MD,
valve
Pts.
twenty-six
pain
of
(pts.)
mitral
4.2).
7 pts.
in
chest
the
excluded.
pts.
hundred
whom
atypical 8
II
UP
Ohio.
47.1).
chordae
surgery
pts.).
Only
in
Ruptured
were
FOLLOW
Moreyra,
attributed
(mean
A
MD; Sergio
Abel
patients of
(mean
heart
(MR).
Lardani,
FACC;
years
from
VALVE;
ANGIOGRAPHY
Cleveland,
nary
time
MD,
prolapse
I-11
MITRAL
BY
thirty-seven
proven
followed
THE
Hector
MD;
Sheldon,
Foundation,
ically
was
OF
STUDIED
pts.
fatal
incidence without
with MR
and of
is
idiopathic
MVP
have
a
associated
with
a
higher
nonfatal sudden
significant
complications death MR.
benign
(73%).
There
(1.7%) in medically