We retrospectively analized 72 patients affected by CAD,
diagnosed by a previous CardiacCT exam,
who underwent Cardiac MR in order to study coronary flow reserve.
According CT exams,
about the 42% of study population showed a hemodinamically significative plaque.
During the first qualitative evaluation of CMR exams,
we identified potential perfusion defects,
at rest or only during stress with adenosine infusion (reversible defects),
or the presence of myocardial scar,
suggestive for underlying myocardial infarction.
Thank’s to this first evaluation,
we differentiated our study population in two different class: 1.
Ischemic or infartuated patients (respectively,
those who showed inducible ischaemia,
with reversible perfusion defect and those with stable ischaemia,
perfusion defect not correlate with adenosine infusion and myocardial scar); 2.
Non ischaemic patients (apparentely health patients,
without any perfusion defects).
Then we calculated T1 mapping values with a dedicate software (Circle 42®) at rest,
during adenosin infusion and after 15 minutes from the last gadolinium injection,
on septal and anterior wall,
in order to assess the T1 reactivity in all patients,
T1 reactivity is the increase of T1 values during adenosine infusion; in fact,
as reported in literature,
an increase of myocardial perfusion,
such as during adenosine infusion,
correlate with the increase of myocardial water content which prolong T1 relaxation times; hence,
adenosine infusion cause an increase of myocardial T1 values (called T1 reactivity)6.
However,
T1 myocardial value could change in response to other pathologic conditions as oedema or increase of extracellular space like in presence of myocardial fibrosis due to myocardial infarction7; furthermore,
T1 values measured before and after gadolium administration,
on myocardium and on blood pool,
permits to calculate Extra-Cellular Volume (ECV) value8.
ECV measures the volume of distribution of gadolinium9,
which spreads into the interstitial space withouth pass the citoplasmatic membrane.
Normal values of ECV are about 25± 3.5%.
ECV values more than 32% are suggestive for extracellulare volume expansion due to increase of water content or fibrosis (collagene deposits)10.
So,
increase of ECV value reflect the same T1 value change due to myocardial fibrosis,
as markers of myocardial remodelling11.
The 38 ischemic/infartuated patients,
as expected,
showed hight T1 myocardial value at rest,
probably due to extracellular space change (1,300.12±68.36ms to 1412,48±58ms in infartuated patients),
with no significative reactivity during adenosine infusion (p-value: 0.305),
and an ECV value of 35,4%,
in agreement with previous literature6.
15 of 34 non-ischaemic patients,
as healthy patients,
showed normal T1 myocardial values at rest (1102±42ms at rest),
with significative responsivity during adenosine infusion (p value: 0,0167) and a normal ECV value (23%).
The remaining 19 non-ischemic patients,
however,
showed T1 values change similar to ischaemic/infartuated patients,
even without perfusion defect or myocardial scar [T1 mapping at rest (1301±44ms),
with no significant modification during stress (p value: 0,21) more than normal values (29,9%)] (fig.
5).
These T1 values changes in apparentely healthy patients could be due to microvascular disfunction,
as supposed by Arnol et al12,
or to early myocardial remodelling not assessable with other CMR sequences,
as Perfusion or LGE sequences.
Hence,
T1 mapping and ECV sequences could result more sensitive and specific sequences in identification of early myocardial changes respect to conventional qualitative evaluation.