*From the Cardiology Department, Heraklion University Hospital, Heraklion, Crete, Greece.
Correspondence to: Panos E. Vardas, MD, PhD, Cardiology Department, Heraklion University Hospital, P.O. Box 1352 Stavrakia, 71110 Heraklion, Crete, Greece
A 52-year-old patient underwent percutaneous balloon
pericardiotomy because of rapid fluid accumulation. During the
procedure, we calculated the amount of blood flow to the nondiseased
left anterior descending coronary artery while pericardial pressure was
gradually increased by the infusion of warmed normal saline solution.
Coronary vasodilator reserve was assessed by intracoronary adenosine.
With increasing pericardial pressure, there was a continuous decline in
coronary blood flow, due to an increase in coronary vascular
resistance, and an unaffected hyperemic response throughout. The
maximal hyperemic flow was far less under increased pericardial
pressure than at normal pressure, which implies an augmented
susceptibility to myocardial
the fact that pericardial pressure has been clinically diagnosed since
the 19th century, and that numerous reflexes and systemic
cardiovascular effects have been well described, only a very few
studies have dealt with its effects on coronary blood flow, and these
used experimental animal models.
Based on animal studies, previous authors have concluded that
with an increase in pericardial pressure there is a continuous decline
in coronary blood flow, with a reduction of approximately 50% during
cardiac tamponade, but controversy exists about the underlying
mechanism. Abel et al1suggested that in dogs this
reduction was due to a decrease in perfusion pressure, as shown by the
lack of significant change in coronary vascular resistance. In
contrast, Bernath et al2suggested that anα
-adrenergic mechanism was responsible, while Kingma et
al3 found that vascular resistance is increased in the
subendocardium at high pericardial pressures.
In view of the lack of data for humans, we present here the
first report of the effect of pericardial pressure on human coronary
circulation. These data are taken from a 52-year-old patient with lung
cancer and cardiac tamponade who was successfully managed with
pericardiocentesis, during which 850 mL hemorrhagic fluid was removed.
Because of rapid fluid accumulation the patient was scheduled for
percutaneous balloon pericardiotomy 5 days later. During that
procedure, we calculated blood flow to the nondiseased left anterior
descending coronary artery with increasing pericardial pressure
achieved by the infusion of warmed normal saline solution at a rate of
30 mL/min. The patient was informed about the procedure and gave his
A 0.014-inch, 15-MHz guidewire (FloWire; Cardiometrics;
Mountain View, CA) was used to measure coronary flow velocity in the
left anterior descending coronary artery, and the quantitative flow was
calculated as the product of the vessel cross-sectional area and half
of the time-averaged peak coronary flow velocity.4
Coronary vasodilator reserve was assessed by intracoronary
administration of 18 μg adenosine to induce maximal hyperemia.
Measurements were made after each 60-mL infusion into the
pericardial space. The study was terminated because of chest discomfort
after 205 mL saline solution had been infused.
shows the coronary blood flow velocity for minimum and maximum
pericardial pressure, at baseline and at maximal hyperemia. The effect
of the increase in pericardial pressure on the coronary and peripheral
hemodynamic parameters measured is shown in Table 1
. Perfusion pressure was defined as mean arterial pressure minus
pericardial pressure, and coronary flow reserve was defined as the
ratio of coronary blood flow at maximal hyperemia to that at baseline.
Clearly, there was a marked progressive decrease (47%) in coronary
blood flow with the increase in pericardial pressure even
though perfusion pressure showed a small decrease (8%). This was due
to a progressive increase in coronary vascular resistance, which also
was marked (72%). These changes did not affect the coronary
vasodilator reserve, which remained almost constant in each phase of
the study. Another interesting finding is that of retrograde systolic
coronary flow, which became more pronounced with increasing pericardial
pressure and could perhaps be explained by the degree of pericardial
constriction from the neoplastic process.5
In conclusion, with increasing pericardial pressure
there is a continuous decline in coronary blood flow due to an increase
in coronary vascular resistance and an unaffected hyperemic response
throughout. The maximal hyperemic flow is far less under increased
pericardial pressure than at normal pressure, which implies an
augmented susceptibility to myocardial ischemia.
Peri Pr = pericardial pressure; HR = heart rate;
AP = arterial pressure; Perf Pr = perfusion pressure;
CBF = coronary blood flow; CVR = coronary vascular resistance;
CFR = coronary flow reserve.
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