K. T. WEBER, R. A. RATSHIN, C. E. RACKLEY AND R. 0. RUSSELL, JR. 
173 
(60). 
15 20 25 30 35 W 
PA or LVEDP 
Figure 3. — A plot of cardiac index versus left ventric- 
ular filling pressure (mmHg expressed by pulmonary 
artery or left ventricular end diastolic pressure). 
The open symbols represent survivors and the closed 
symbols represent those patients which died. Tri- 
angles are representative of those patients with in- 
ferior myocardial infarction; circles represent those 
with anterior myocardial infarction; and squares 
represent those patients having left bundle branch 
block. 
When three patients with LBBB were included, 
the mortality was 98 % . In six patients with CI 
less than 2.1 and LVFP less than or equal to 15, 
66% died. The four patients with CI greater 
than or equal to 2.1 regardless of LVFP had 
only a 36 % mortality. 
In Group B, mean HR was 94 (56-127) ; SI 
28 (12-54) ; CI 2.46 (1.2-4.1) ; PVR 55.4 (25- 
129) and LVFP 20 (2-50). The mean hemo- 
dynamic values seen in Group B are similar to 
the findings in Group A with the exception of 
SI, which is substantially lower in Group A. 
This represents an approximate 60% and 38% 
reduction from normal (45 cc/m^) in SI for 
Groups A and B, respectively. Accompanying 
medical complications (angina, previous infarc- 
tion, congestive failure and hypertension) did 
not influence the presenting hemodynamics in 
Group A or B. 
Experimental 
The results of the slow (4- to 6-hour) micro- 
sphere infusion method^ in nine animals are 
shown in Table II. In the low dose group (ani- 
mals 1 through 4; 4 mg/kg body weight) the 
primary hemodynamic abnormality at rest was 
the persistently elevated LVEDP. Flow and 
pressure characteristics of the heart were other- 
wise generally within the limits of normal for 
these animals.- The high dose group had sev- 
eral abnormal findings at rest including reduc- 
tions in stroke volume, cardiac output, mean 
injection rate and rate of LV pressure rise. 
LVEDP was elevated chronically as in Group I. 
During angiotensin stress (Fig. 4), both groups 
demonstrated abnormal responses. This was 
particularly evident in Group II. Heart weight 
and wall thickness were increased 65% and 
45%, respectively, above normal- for both 
groups. 
Of particular note with this technique of slow 
microsphere embolization is the lack of ven- 
tricular arrhythmias during the infusion pe- 
riod. All animals, except 3 and 7, were elec- 
tively sacrificed. These two animals died at 
three days postinjection with thrombosis of 
the left main coronary artery surrounding the 
infusion cannula. The histopathology in all ani- 
mals demonstrated widespread cellular death 
and injury throughout the left ventricle at var- 
ious states of development.^' 
Those animals receiving similar doses of mi- 
crospheres (also 6-14 micron in diameter) but 
infused over 15 to 30 minutes, demonstrated a 
totally different response. In this series, stable 
hemodynamic shock was dominant with or with- 
out elevations in LVEDP. The average results^ 
are presented in Table III. In addition, three 
of the seven animals died with irreversible ven- 
tricular fibrillation. Two others had electro- 
mechanical dissociation unresponsive to phar- 
macological support. 
Major vessel occlusion representing 25% to 
40% reduction of left main coronary flow in 
conscious animals resulted in hemodynamic and 
