Author + information
- Ioana M. Dregoesc, MD,
- Adrian C. Iancu, MD, PhD∗ (, )
- Tudor Cucu and
- Mãdãlin C. Marc, MD
- ↵∗Department of Cardiology, “Iuliu Haţieganu” University of Medicine and Pharmacy, 19-21 Calea Moţilor, Cluj-Napoca 400001, Romania
“A rose tree may be a rose tree may be a rosy rose tree if watered” (1). As such, the index of microvascular resistance (IMR) is associated with microvascular pathologies, including microvascular obstruction (MVO). If “watered,” however, IMR associates with edema and inflammation and therefore the condition of the tissue becomes more than simply obstructive. But is IMR as powerful a negative parameter as Bulluck et al. (2) have presented it to be? Unlikely.
Recently, Patel et al. (3) have demonstrated that pressure at zero flow (Pzf) is the most sensitive invasive coronary physiology index currently available for the assessment of microcirculation at the time of primary percutaneous coronary intervention. It predicts the final extent of global and regional irreversible myocardial injury and left ventricular function at 6 months. Pzf is significantly more useful than IMR (3).
In the setting of noncollateralized occlusions, coronary wedge pressure (CWP) is similar to Pzf, as both of them are pressure measurements at ceased coronary flow. However, Pzf is a theoretical hemodynamic parameter that measures coronary pressure at zero flow. This never happens in a beating heart. IMR and Pzf are difficult to measure during percutaneous coronary intervention and the measurement is time consuming. This is not true for CWP, which is easily determined. CWP is the distal pressure in the occluded vessel after the occlusion is wired. The measurement is done through microcatheters and it reflects all the events that precede the revascularization procedure.
In the infarcted wall, MVO could impede coronary blood ejection into the venous circulation. This increases CWP by means of a large and tall systolic wave that defines the hemodynamic spectrum of MVO. On the other hand, CWP is also influenced by interstitial pressure as interstitial edema compresses capillaries and increases the intravascular pressure. The edema and inflammation surrounding the infarct zone are important determinants of left ventricular remodeling. A new coronary wave flow configuration occurs, with continuous elevation of the pressure line.
In the first scenario, the high CWP suggests the embolism and the MVO. It also identifies the group of patients most likely to benefit from intracoronary glycoprotein IIb/IIIa inhibitors or thrombolysis. The use of microcatheters allows a high drug concentration to be established through downstream intracoronary delivery. The drug is injected distal to the occlusion hereby avoiding the use of a guide for administration, which is ineffective.
In the second scenario, edema and inflammation are secondary to inflammatory cell embolism arising from inflammatory cell-rich old thrombi. Probably these patients would benefit more from anti-inflammatory therapy.
The use of micro-catheters before reperfusion can more accurately define thrombus burden and the length of the lesion by small dye injection. This simple procedure allows for direct stenting and avoids pre-dilatation in an era where thrombus aspiration failed to prove beneficial.
There are several scenarios regarding tissue damage in ST-segment elevation myocardial infarction. One such scenario concerns the embolism that occurs several days before the onset of symptoms and it was recently described by De Maria et al. (4) and suggested by Kramer et al. (5). Moreover, post-mortem studies on patients who died of non-revascularized acute coronary syndromes revealed that micro-emboli and inflammatory surroundings were more common in this subset of cases, clear proof of severe pre-procedural intramyocardial damage. As Mahmoud and Zijlstra (6) stated in a recent review, in ST-segment elevation myocardial infarction, “distal embolization and microvascular obstruction might already have occurred to some extent before admission.”
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
- Stein G.
- Bulluck H.,
- Foin N.,
- Carbrera-Fuentes H.A.,
- et al.
- Patel N.,
- Petraco R.,
- Dall'Armellina E.,
- et al.
- De Maria G.L.,
- Cuculi F.,
- Patel N.,
- et al.
- Kramer M.C.,
- van der Wal A.C.,
- Koch K.T.,
- et al.
- Mahmoud K.D.,
- Zijlstra F.