Increased Angio-Derived Index of Microcirculatory Resistance Within a Timeframe of 30–60 days After COVID-19 Infection, 2024, Dong et al.

[SNT Gatchaman]

Increased Angio-Derived Index of Microcirculatory Resistance Within a Timeframe of 30–60 days After COVID-19 Infection
Lei Dong; Ritai Na; Lang Peng; Xinye Xu

BACKGROUND AND OBJECTIVES
Chest pain is a relatively long-term symptom that commonly occurs in patients who have contracted COVID-19. The reasons for these symptoms remain unclear, with coronary microvascular dysfunction (CMD) emerging as a potential factor. This study aimed to assess the presence of CMD in these patients by measuring the angio-derived index of microcirculatory resistance (AMR).

METHODS
In this cross-sectional case–control study, patients who had chest pain and a history of COVID-19 infection within the preceding 30 to 60 days were included. The control subjects were patients without COVID-19. Demographic, clinical, and echocardiographic data were recorded. Angiographic images were collected for AMR analysis through an angioplus quantitative flow ratio measurement system. Propensity score matching (PSM) was performed to match the two groups. Multivariate logistic regression was used to examine the association between COVID-19 incidence and the increase in AMR (AMR > 285 mmHg*s/m) after correction for other confounders.

RESULTS
After PSM, there were 58 patients in each group (the mean age was 66.3 ± 9.04 years, and 55.2% were men). The average time between the onset of COVID-19 infection and patient presentation at the hospital for coronary angiography was 41 ± 9.5 days. Moreover, there was no significant difference in the quantitative flow ratio between the two groups.

Patients with COVID-19 had a greater mean AMR (295 vs. 266, p = 0.002). Multivariate logistic regression analysis revealed that COVID-19 (OR = 3.32, 95% CI = 1.50–7.60, p = 0.004) was significantly associated with an increase in AMR.

CONCLUSIONS
Long-term COVID-19 patients who experience chest pain without evidence of myocardial ischemia exhibit an increase in AMR, and CMD may be one of the reasons for this increase. COVID-19 is an independent risk factor for an increase in AMR.

Link | PDF (Microcirculation)

 

[John Mac]

Is this more evidence of Endothelial dysfunction in Long Covid?

 

[SNT Gatchaman]

In the present study, we demonstrated for the first time the relationship between COVID-19 and an increase in AMR. Patients with COVID-19 had a greater mean AMR, and the results of the multivariate logistic regression analysis showed that COVID-19 was an independent risk factor for an increase in AMR after correcting for other confounding factors.

our results revealed an increase in the AMR in patients who experienced chest pain and had a history of COVID-19 infection, despite the absence of severe stenosis in epicardial vessels during coronary angiography. This suggested the potential presence of CMD [coronary microvascular dysfunction].

Several studies have been conducted to date to assess coronary microcirculation in patients with COVID-19. Çalışkan et al. assessed the status of coronary microcirculation by measuring coronary flow velocity reserve (CFVR) via echocardiography. These findings indicated a lower CFVR in patients with COVID-19. Consequently, it can be inferred that COVID-19 affects coronary microcirculation. The primary indicator for evaluating coronary microcirculation is the index of microcirculatory resistance (IMR).

While the IMR measurement is relatively accurate, the intricate procedure and the high-cost pressure–temperature sensor guidewire pose significant hurdles for the routine implementation of this technology. These limitations have limited the sample size of research using the IMR as a criterion. Moreover, all of these methods require the use of vasodilator drugs, such as adenosine, which may induce hypotensive reactions or lead to patient intolerance.

The AMR represents an emerging index for evaluating coronary microcirculation function. It is calculated through artificial intelligence modeling applied to coronary angiography images.

 

[SNT Gatchaman]

The results of the present study also revealed an increase in AMR among long-term COVID-19 patients. This finding suggested that COVID-19 might impair coronary microcirculation, consistent with prior research findings. Coronary microcirculation refers to coronary vessels with a diameter less than 500 μm. Microcirculatory function is important for myocardial perfusion.

Systemic inflammation and immune responses induced by COVID-19 lead to vascular endothelial damage and thrombosis, compromising coronary microcirculatory function. COVID-19 targets angiotensin-converting enzyme 2 (ACE2) receptors on the surface of vascular endothelial cells, directly damaging endothelial cells. Additionally, COVID-19 induces a cytokine storm, generating substantial amounts of proinflammatory cytokines that activate endothelial cells. Consequently, these activated endothelial cells release von Willebrand factor (vWF) multimers, which bind to platelets and contribute to the formation of microthrombi, impairing microcirculatory function.

There are several limitations in this study. First, the criteria of AMR used for determining CMD after long-term COVID-19 are unclear. Additionally, the accuracy of AMR measurements is confounded by factors such as image quality and projection angle. Further studies can be designed to combine symptoms and the IMR to further optimize the methodology. Second, this was a single-center study with a small sample size and a cross-sectional design. The present findings do not show that COVID-19 causes an increase in AMR but rather suggest an association between them. Third, this was a retrospective study, and further prospective studies, such as RCTs, need to be designed to explore the value of the AMR in guiding clinical practice. Finally, AMR is a new method, and only a few studies have reported the reliability of this method compared with conventional IMR measurements.

 

[Dolphin]

I wonder whether a similar thing happens with the chest pain in ME/CFS. I remember getting it first as a teenager. I wondered was a heart attack but figured I was probably safe given my age and that I wasn’t overweight and had never been overweight.