Pulsatile flow
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Vanessa Cherniauskas, M.D. [3]
Synonyms and keywords: Pulsatile blood flow pattern; pulsatile pattern; pulsatility; systolic flow reversal
Overview
The presence of a pulsatile flow pattern (systolic flow reversal) in epicardial coronary arteries is associated with slower flow with impaired myocardial perfusion and adverse cardiovascular outcomes. Pulsatility signifies an increased vascular resistance and may be used for risk stratification on coronary angiography.
Definition
Pulsatile flow is defined as flow reversal with intermttent cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole.[1] It is coded as yes (present) or no (absent).
Pathophysiology
Pulsatile flow is associated to a reduced ST-segment resolution and an impaired myocardial perfusion which may be explained by distal embolization and the release of vasoconstrictors. Furthermore, a visible intracoronary thrombus is more commonly present among arteries with a pulsatile flow pattern.[1]
Since LAD was the most common culprit vessel we can observe that infarcts in these patients are characterized by a greater volume of myocardium distal to the stenosis[2]. It is also noticed a thicker myocardium compared to the right ventricle, and a higher left ventricular filling pressure compared to the right ventricular filling pressure. Thus, the pulsatile flow is seen as a result of the greater myocardial edema and also due to the consequent extrinsic compression of the capillary network as well as the higher left ventricular filling pressure which is developed among patients with anterior infarction. Moreover, it is important to emphasize that the systolic flow reversal occurs when the downstream microvascular pressure during systole exceeds the upstream epicardial artery pressure which causes abnormalities in the downstream microvasculature, some of which may be mediated by heightened noradrenergic tone to maintain the perfusion pressure. This tone is relieved after dilation of the stenosis which means that if the pressure beyond the stenosis is low, heightened pressure during systole may cause flow to reverse in this low pressure system explaining, accordingly, the mechanism of occurrence of the pulsatile flow. Finally, it is possible to declare that pulsatile flow is associated with larger infarct areas reflected by their larger peak creatine kinase levels. However, the directionality of the causal relationship is unknown once it is not clear until now if the larger myocardial infarctions are the cause of pulsatile flow or if pulsatile flow, which represents a surrogate for heightened downstream microvascular resistance, in turn, is responsible for larger myocardial infarctions.[1]
Example
Clinical Significance
- Pulsatile flow pattern can be considered as a surrogate for exalted microvascular resistance. It may also be observed in other conditions such as ventricular hypertrophy. Patients with TIMI flow grade 2 were shown to have a greater incidence of pulsatile flow compared to those with TIMI flow grade 3.[3]
- The presence of pulsatile pattern in the infarct related artery is reported to be associated with an increased incidence of pulsatile flow in nonculprit arteries and also with a slower nonculprit flow.[2]
- In a pooled retrospective cohort study on patients with acute myocardial infarction, a pulsatile pattern in epicardial flow was associated with higher corrected TIMI frame counts (CTFC), lower TIMI myocardial perfusion grades (TMPG), less complete ST-segment resolution, higher peak creatine kinase, and elevated risk of reinfarction and death at 30 days.[1] In addition, patients treated with combination therapy of glycoprotein IIb/IIIa inhibitor and fibrinolytic agent less frequently had pulsatile flow compared with patients treated with fibrinolytic monotherapy.
References
- ↑ 1.0 1.1 1.2 1.3 Gibson, CM.; Karha, J.; Murphy, SA.; de Lemos, JA.; Morrow, DA.; Giugliano, RP.; Roe, MT.; Harrington, RA.; Cannon, CP. (2004). "Association of a pulsatile blood flow pattern on coronary arteriography and short-term clinical outcomes in acute myocardial infarction". J Am Coll Cardiol. 43 (7): 1170–6. doi:10.1016/j.jacc.2003.11.035. PMID 15063425. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Gibson, CM.; Murphy, S.; Menown, IB.; Sequeira, RF.; Greene, R.; Van de Werf, F.; Schweiger, MJ.; Ghali, M.; Frey, MJ. (1999). "Determinants of coronary blood flow after thrombolytic administration. TIMI Study Group. Thrombolysis in Myocardial Infarction". J Am Coll Cardiol. 34 (5): 1403–12. PMID 10551685. Unknown parameter
|month=ignored (help) - ↑ Gibson, CM.; Murphy, S.; Menown, IB.; Sequeira, RF.; Greene, R.; Van de Werf, F.; Schweiger, MJ.; Ghali, M.; Frey, MJ. (1999). "Determinants of coronary blood flow after thrombolytic administration. TIMI Study Group. Thrombolysis in Myocardial Infarction". J Am Coll Cardiol. 34 (5): 1403–12. PMID 10551685. Unknown parameter
|month=ignored (help)