C4
SEPTEMBEFA
0
VOL. 50
Circuta lion
1974
NO. 3
AN OFFICIAL JOLURNAL of the AMERICAN HEART ASSOCIATION
EDITORIAL
Di Si Dolce Morte
It May Be Safer To Be Dead Than Alive
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EXPERIENCED CARDIOLOGISTS have long
recognized that_~the patient who has had one or
more heart attacks carries a greater hazard of sudden
or, more specifically, instantaneous death. Even
Leonardo da Vinci* recognized the association of
severe coronary artery disease and instantaneous
death, although he probably had never heard of a risk
factor. More recent and more sophisticated studies,
including long term electrocardiographic monitoring,
have indicated that recurrent premature ventricular
complexes (PVCs) constitute a powerful risk factor for
death in patients who have had a myocardial infarction.2' Interestingly enough, PVCs do not constitute
a risk factor for nonfatal myocardial infarction.2 It
must be remembered that so-called risk factors are
epidemiologic associations, not necessarily indicative
of an etiologic relationship. The demonstration that
PVCs are associated with a higher risk of death does
not prove that the prevention of PVCs will decrease
the incidence of death.
Attempts to protect the high risk patient with antiarrhythmic agents have not been convincing; indeed, the bulk of the evidence at hand indicates that
thev cannot be so protected even though the PVCs
Is this an inadequacy of the
may be eliminated.4'
Froin
therapeutic program? It may be. Currently available
drugs are difficult to use in effective dosage over long
periods of time. An alternate possibility exists. It may
be that both the PVCs and sudden death may relate to
a common cause, so that one does not necessarily
followv the other. If they have a common cause, not
stifled by available antiarrhythmic therapy, it is
probably related to an electrically unstable ischemic,
but not dead, area of the heart tissue. If this is true,
the hazard of sudden death might be lessened by
either relieving the ischemia, killing the unstable
tissue, or possibly isolating it from all potentially disturbing stimuli.
In the light of this avenue of thinking, the recent
report bv Cobb and his associates is most interesting.6
In the large Seattle experieince with mobile coronary
thev have studied a group of patients with
care,
primary ventricular fibrillation,' who suffered the
tunheralded onset of ventricular fibrillation. In the
Seattle svstem, a number of such people have been
resuscitated and their long term survivial studied. Of
great interest, those patients who develop classic
evi(lence of myocardial infarction in the postrestuscitation period have a better survival rate over
the next two vear period than those who have no
evidence of infarction. Patients of this type have
demonstrated that they have the potential of developing lethal ventricular fibrillation; yet if they have
an infarction, they do better in the long run. Could it
be that the arrhythmia-producing focus has been
killed?
From another direction, we are hearing much diseussion of the benefits or lack of proven benefits
follow, ing bypass surgery on the coronary arteries.
Mlanx patients wx ith angina pectoris appear to be improvecl, but is life prolonged? Perhaps an ischemic
focus is rendered less ischemic and, therefore, is less of
the Department of \ledicine, The Ohio State Universitx,
C)olunbus, Ohio.
\ddress for reprints: James V. Warren, \l.D., Professor and
(Chirnlmm Department of \Iedicine, The Ohio State University,
410 Ws est 1Oth \Aenue, Columbus, Ohio 43210
le \s as talking to an1old man who suddenly sat up and ithout
an moo (enient or signi of ans thing amiss, he passed aw ay from this
life l cnardo carrie(l out anl autopsy to findl out la causa di si
olce morte (the cautse of so gentle a death) and fotund -that it
pmocceded from sweakness through failure of the blood and of the
arterv that fee ds the heart and the other memhers s hich I found to
be v erv p)archle(l anid shrunk anid smithered.1
-
415
Circulatiomn Vo0/lotne
.0,
September 197-4
EDITORIAL
416j
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a hazard. Another possibility has been suggested that
the surgical procedure converts an ischemic, painful,
and arrhythmia-producing area of heart into a dead
infarcted area. The area of dead tissue need not be
great. Some have said that the bypass procedure may
in fact be controlled myocardial infarction.
We are considering here what the epidemiologists
call secondary prevention. The initial clinical event
has already taken place, and we are focusing
specifically on sudden death, not myocardial infarction or angina pectoris. The NIH Coronary Drug Project has indicated that the classic risk factors in this
situation, such as hypertension or lipid abnormalities,
become far less powerful when compared with new
ones such as arrhythmia, heart failure, cardiomegaly,
electrocardiographic abnormalities, or even intermittent claudication." 4 These new factors are, in effect,
measures of the damage caused by the vascular disease. It is not inconsistent with these facts that a small
irritable focus of activity may remain ischemic but not
infarcted, as a virtual firecracker ready to go off in the
heart if its fuse is ignited.
Heavy cigarette smoking presents an interesting additional factor to be considered. Although recognized
by most as an important risk factor, its behavior has
been capricious. Its role is probably multi-factorial.
Heavy smoking creates excess carboxyhemoglobin
and in turn modest polyeythemia. It has also been correlated with high levels of catechol activity. The
Framingham Study showed a positive association
between cigarette smoking and sudden death.7
Studies of a small group of patients at the Ohio State
University Hospitals, coronary care unit have shown
an interesting possible correlation between smoking
habits, catechol excretion, and lethal arrhythmias.8
Sudden arrhythmic deaths appear to be more common in those patients with a history of cigarette smoking which is correlated with high catechol amine
levels. It raises the question of the humoral environment of the ischemic tissue. Circumstantial evidence,
to be sure, but interesting in light of the other factors
apparently associated with sudden death.
Instantaneous death is clearly electrical, but what is
it that fires it off? It would appear to come from
ischemic, but not dead tissue. Although the studies
quoted here make a sharp distinction, one's ability to
distinguish live or dead tissue is, at times, rather arbitrary, as indicated in a recent paper in this journal.9
For our purposes here, live tissue is electrically active
tissue, and abnormally so in becoming the focus of
developing ventricular fibrillation. Undoubtedly the
humoral environment surrounding the ischemic tissue
must play a role; hence, the interest in catechol amines
and their relationship to smoking.
Short of prevention of the underlying problem,
drugs appear to be the simplest means of control. We
desperately need more powerful antiarrhythmic
drugs. Perhaps the FDA, rather than spending all of
its efforts in the regulatory scrutiny of new drugs,
should also stimulate the development of new drugs.
If not directly antiarrhythmic, perhaps an effect
reducing the impact of catechol activity may be
desirable.
If we cannot suppress the potentially lethal electrical activity, should we trv to kill the focus of
irritabilitv? Perhaps new surgical means of isolating
the sensitive focus can be developed.
In the meantime, the expert clinician recognizes the
great hazard present in the unstable and irritable
mvocardium of certain stages of coronary artery disease. The Cobb data suggest that having the ventricular irritability temporarily as the result of an
acute infaretion, rather than chronically, may be the
lesser of two evils. It may be that such patients might
have available self-medication as described by Sarnoff,'0 and thev certainly should be aware of the early
coronarv care services in their community. These can
help even if the "'death' is instantaneous as illustrated
by experience in Seattle,6 Columbus," and other
cities. Above all, we need true prevention. In terms of
risk factors, dead tissue in limited amounts may be
safer than live irritable tissue.
J\MES V. WA\BREX, M.D.
References
1 CX ni o R: Leonardo & The Age of the Eve. Nexv York, Simon
and Schuster, 1970
2. Tin C:om.- Di.u. PiioJF(--i Gioi[-i: Prognostic importance
of premature beats following myocardial infarction, experience of the coronarv drug project. JAMA 223: 1116, 1973
:3. HNKi.I. ILE, C.xiix,F i ST, Aii(m n-os DC: The prognostic
significance of ventricular premature contractions in healthy
people and in people vvith coronary heart disease. Acta Cardiologica: In press
4. \IoS C: Sudden coronary death: The nature of the problem.
The Cooper Colloquium. Wayne, New Jersey, Cooper
Laboratories, Inc.
5. Los ii RRH, Pnii.\Fx.s RJ: Mechanisms of sudden death and
their implications for prevention and management. Prog
Cardiovasc Dis 8: 482, 1971
6. Co(i LA, \i .\xBFEz H, B.st- RS: Sudden cardiac death: The
role of 'primary' ventricular fibrillation. Proceedings of the
Association of Universitv Cardiologists, Phoenix, January
1974
7 Tmll Fit sIxu(.u xsi S-iuit : An epidemiological investigation of
cardiovascular disease. XIII: Incidence of sudden death from
coronar, heart disease by sex, age, and level of characteristic
at examination for 22 characteristics. Washington, D.C..
U.S. Governmerrt Printing Office, 1968
8 BOt u)t .i xs H, LFEWl s RP, FoRESTi Fi1 W, WISS LEB AM:
Adrenergic activity and early arrhythmias in smokers and
nonsmokers sith acute mvocardial infarction. Am Heart J:
In press
9. RLou iso'. RR, N;.Ei. EL, Hins uxi xx JC, NU.SSFNFELFD SR,
Circuilation, Volume 50, September 1974
EDITORIAL
417
Bi-\( Kiiot. ri\ BD, D \x l.i JH: Pathophysiologic observations
in prehospital ventricular fibrillation and sudden cardiac
death. Circulation 49: 790, 1974
SJ: Carl J. Wiggers Award Lecture. American
10. Sul
Phvsiological Society, Atlantic City, New Jersey, 1970
11. Li " l RP, W\HiO: JV: Factors determining mortality in the
pre-hospital phase of acute myocardial infarction. Am J Car(liol 33: 152, 1974
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Correction
I
page 135, the first sentence should read, "For such patients
1974.
On
Mirsky et al.: Circulation 50: 128,
the method must be modified by performing biplane studies and quantitating segmental pressure-volume
curves.
Also on page 135, in Appendix 1, the constants al, 01, and a2 are:
a1 = 3 - h/B - h/2A + h2/2B2
dl = h/A + 2h/B
aZ2 = (h/B) (1 - h/2B + h2/4B2) + (h/2A) (1 - h/2A)
Circulation, Voluine 50, September 1974
Di Si Dolce Morte: It May Be Safer To Be Dead Than Alive
JAMES V. WARREN
Circulation. 1974;50:415-417
doi: 10.1161/01.CIR.50.3.415
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