Short Term and Long Term Complications after Percutaneous Transluminal Coronary Angioplasty
Ganesh N. Sharma*
*School of Pharmaceutical Sciences, Jaipur National University, Jaipur (Raj.)- India
Background: The nonsurgical treatment of arteries narrowed by atherosclerosis was introduced in 1964, when Dotter and Judkin
performed transluminal angioplasty of femoral artery stenoses. In 1970, Gruntzig modified the dilation catheter to allow its use in
coronary arteries dilation . Subsequently, In 1977 he performed the first Percutaneous Transluminal Coronary Angioplasty (PTCA)
in a patient. Since onward, PTCA has been used in many patients with stable angina, unstable angina or acute myocardial infarction. Its
use was initially limited to the treatment of discrete stenoses in proximal segment of a coronary artery, but improvements in equipments
and techniques have lead its use in patients with stenoses, that are more complex or located in distal arterial segments and in patients relatively
at high risk for complications. Despite the wider application of PTCA, the success rate remained high. Over the past decade,
the number of procedure performed has steadily increased, with over 300,000 performed in united state in 1990.
Short- Term Complications
Although PTCA is genrerally safer, complication occasionally occurs
including myocardial infarction in 3 to 5 percent [5,6], Yet
it is need for emergency bypass surgery in 3 to 7 percents [7,8]
and death in 0 to 2 percent [9,10]. These event usually caused by
extensive coronary arterial dissection, intracoronary thrombosis,
or both, with resultant vessel occlusion. Coronary arterial perforation,
rupture, or remobilization is rare. The last is more likely in a
sphenous- vein graft than in a native vessel.
Acute or abrupt closure occurs in 2 to 8 percent of patients undergoing
PTCA [11,12], and accounts for most of the short – term
morbidity and mortality associated with the procedure. In about
75% of patients with abrupt closure, it occurs within minutes after
PTCA, when they are still in the catheterization laboratory; in the
other 25 percent it usually occurs within 24 hours after the procedure
Mechanism of Abrupt Closure
Three pathophysiologic processes may contribute to the occurrence
of abrupt closure after PTCA: extensive dissection, thrombosis,
and coronary vasospasm . Some degree of intimal dissection-
characterized angiographically as a linear interaluminal
filling defect or flap associated with a hazy, ground glass appearance-
is frequently observed after successful PTCA. When the dissection
is limited, its angiographic characteristics may be subtle
and evident only on selected views. However, when it is extensive,
the radiographic features are readily apparent, and the vessel lumen
may be compromised. 10 % of patients with coronary arterial
dissection after PTCA require emergency bypass surgery, sustain a
myocardial infarction, or die. In contrast, less than 2 % of patients
without extensive dissection have a serious complication .
Acute thrombus formation after PTCA is characterized angiographically
as an intraluminal filling defect or an area stained with
radiographic contrast material. Thrombus formation is most likely
to occur in patients with extensive dissection, those with a severe
residual stenosis after PTCA, those with pre-existing intracoronary
thrombus, and those not receiving an antiplatelet agent. In
One study, 22% of the patients undergoing PTCA without antiplatelet
therapy had thrombi, demonstrable by angiography after
dilation. In half of these patients, the thrombi caused occlusion,
requiring repeated PTCA, bypass surgery, or thrombolysis .
Conversely, those who received aspirin before PTCA were much
less likely to have demonstrable thrombi afterward. Since; most
patients receive nitrates, calcium-channel blockers, or both before,
and after PTCA, coronary vasospasm is an uncommon cause of
Risk Factors for Abrupt Closure
Several clinical, anatomical, and procedural variables are associated
with an increased incidence of abrupt closure after PTCA. The influence of these variables is cumulative: the more variables that
are present in a particular case, the greater the likelihood of abrupt
Consequences of Abrupt Closure
The consequences of abrupt closure vary widely. Patients with adequate
collateral perfusion of the occluded vessel may have abrupt
chest pain, electrocardiographic abnormalities, or hemodynamic
compromise. More commonly, abrupt closure is accompanied by
chest discomfort and electrocardiographic evidence of ischemia
and requires immediate revascularization of the occluded vessel to
prevent or limit myocardial injury.
The common Variables associated with an increased risk of abrupt
closure of the artery in patients undergoing PTCA may be clinical,
such as; female sex , unstable angina, MVD or
Anatomical such as; angiographically demonstrable intracoronary
thrombus, eccentric stenosis , stenosis located at or near a
bend or branch, severe pre PTCA stenosis , stenosis or 2 luminal
diameter in length, sequential stenosis, diffusely diseased
artery, procedural variables, extensive coronary arterial dissection
and use of oversized balloon.
Management of Abrupt Closure
Since the most effective treatment of abrupt closure is prevention,
strategies aimed at precluding its possible causes (dissection,
thrombosis, and vasospasm) are routinely instituted. Calciumchannel
blockers, nitrates, or both are usually administered before,
during, and after PTCA, even though no controlled study has
shown that they reduce the incidence of abrupt closure. All patients
receive aspirin before and after PTCA, and all are given heparin
during the procedure, with the adequacy of anticoagulation monitored.
In many centres, patients at high risk of abrupt closure are
given infusion of heparin for 12 to 24 hours after PTCA, although
the efficacy of this approach has not been proved. Only aspirin has
been shown to reduce the incidence of abrupt closure .
When abrupt closure occurs, redilation with a standard balloon
catheter is usually attempted, which is successful in about 50 percent
of patients [ 24]. When this strategy fails, a special balloon
catheter may be used, if the coronary anatomy is suitable. Holes in
the catheter proximal and distal to the balloon allow blood to flow
through the catheter during inflation of the balloon, thus maintaining
perfusion of the distal artery during prolonged inflation. In the
majority of patients in whom a standard balloon catheter fails to
restore sustained anterograde perfusion, a perfusion catheter is effective.
Peripheral vascular complications, such as arterial pseudoaneursym,
laceration, anteriovenous fistula, embolism, arterial occlusion
and hematoma formation, occur in about 3 %t of patients
undergoing PTCA. The use of large arterial sheaths, the concomitant
use of anticoagulant or thrombolytic therapy, an advanced age,
and the presence of peripheral vascular disease increase the risk of
these vascular complications. Other less common acute complications
of PTCA are similar to those of diagnostic coronary angiography,
including arterial or ventricular arrhythmias, conduction
abnormalities, coronary arterial embolization, cardiac tamponade,
allergic reactions to contrast material or one of the medications
given during PTCA, vasovagal episodes, and cerebrovascular embolization
resulting in anuerologic deficit [25, 26].
Long Term- Complications
In patients who have undergone successful PTCA, the chief limitation
on long term, event- free survival is recurrence of the stenosis,
or restenosis. Although improved medical therapy and technical
advances over the past decade have reduced the incidence of abrupt
closure, the incidence of restenosis has not changed. Several definitions
of restenosis have been suggested, but it is most commonly
defined as more than 50 % narrowing of the diameter lumen at the
site previously successful PTCA. Restenosis occurs in about 60%
of those whom a chronically occluded artery has been dialated [27,
28, 29, 30] . Restnosis occurs in one to three month’s afterPTCA,
and in 95 percent of patients, it occurs within six months after the
procedure. Restenosis is uncommon less than one month or more
than six months after PTCA .
Mechanism of Restenosis
The process of restenosis is initiated by injury of the vessel, with
the subsequent release of thrombigenic, vasoactive, and mitogenic
factors . Endothelial and deep vessel injury leads platelet
aggregation, thrombus formation, inflammation, and activation
of macrophages. These events induce production and release of
growth factors and cytokines, which in turn may promote their
own synthesis and release from target cells. Thus, a perpetuating
process is initiated , which results the migration of smooth
muscle cells from their usual location in the arterial media to the
intima, where they change to a synthetic phenotype, produce extracellular
matrix, and proliferate, thereby resulting in a stenosis
within the vessel lumen. In addition, scar contraction may occur,
further reducing the size of the lumen. These processes make up
the wound healing response that occurs in all patients undergoing
PTCA. In patients with the most pronounced reparative response
to the intimal and medial damage induced by balloon inflation,
luminal encroachment is particularly marked, and such patients are
said to have restenosis. Contraction of the dialated and stretched
medial and adventitial layers- so called elastic recoil- may contribute
to restenosis, but such contraction is usually apperent within
hours to days after PTCA .
Risk Factors for Restenosis
Numerous clinical, anatomical, and procedural variables have
been associated with an increased incidence of restenosis after
successful PTCA. The common clinical variables are male sex
, cigarette smoking , diabetes mellitus , hypertension
, hypercholestromia , renal disease, vasospatic angina and
unstable angina [40, 41]. Among the clinical variables, diabetes
mellitus and unstable angina are reported most frequently. The
anatomical variables such as; proximal stenosis, saphenous- vein
graft involvement of the left anterior descending artery, chronically
occluded artery, stenosis more 5 to 10 mm in length, severe pre
PTCA stenosis [42,43,44], and procedural variable such as residual
stenosis, small residual lumen, and used undersized balloon 
may increase incidences of restenosis after PTCA.
Consequences of Restenosis
Most patients with restenosis after successful PTCA have recurrent
angina, but some of those with angiographic evidence of restenosis are asymptomatic. Since such patients have a good prognosis, a
second angioplasty should be reserved for those recurrent symptoms
. Myocardial infarction is rarely the initial manifestation
of restenosis. The severity of narrowing at the site of restenosis is
usually similar to that PTCA. However, when PTCA is performed
in a minimally narrowed coronary artery, the restenosis may be
more severe than initial stenosis.
Management of Restenosis:
Restenosis is often treated successfully with a second PTCA. The
second procedure is more likely to be successful than the first and
less likely to be associated with an acute complication . Probably
a second procedure is performed only in patients in whom
first was successful, and because the restenosis consist primarily
of fibro proliferative tissue rather than atherosclerotic plaque.
Numerous pharmacological approaches and devices have been
evaluated in an attempt to prevent restenosis. Fish oil, and trapidil
(growth inhibitor) have shown promise in some trials [48, 49].
Some trials that failed to demonstrate the benefit of a particular
pharmacologic agent may have too few patients and uses adequate
doses. The incidence of restenosis after elective placement of an
intracoronary stent appears to be low [50, 51], but the result of
randomized trials comparing the use of a stent with PTCA alone
are not yet available.
Since the introduction of PTCA is more than 15 years ago, there
have been notable advances in technique and equipment. Many
stenosis; regardless of their location, severity, or morphologic
characteristics, can now be dilated successfully. The development
of devices should make it possible to expand the use of PTCA even
further. Moreover, new antiplatelet and antithrombin agents may
reduce the incidence of acute thrombotic complications. Restenosis
remains challenge unfortunately; there has been little progress
in reducing its incidence. The physiology of restenosis is multifactorial
and poorly understood. In all probability, therapeutic approach
that several pharmacologic and procedural innovations will
be required to decrease the incidence of restenosis.
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