Title: Innovative angiography: a new approach to discover more hepatic vein collaterals in
patients with cirrhotic portal hypertension
Version: 0 Date: 14 Jan 2023
Reviewer's report:
Major points:
Looking at Figure 4 panel C, it is unclear to me why there was only a small discordance
between WHVP and PP, however, there was substantial discordance between HVPG and PPG.
Since FHVP/VCIP should basically be the same, what is the explanation for this discordance?
The same applies to Figure 6, panel A. Even in Figure 5, differences in WHVP and PP seem
substantially lower than those in HVPG/PPG. How was PPG calculated? If the RAP was used,
it should be exchanged for the VCIP (or FHVP, if VCIP was not measured) – see Baveno VII
recommendations.
Moreover, since sedation/analgesia impacts pressure measurements, the regimens should be
reported. Were the regimens the same when measuring WHVP and PP, or was sedation/analgesia
added/increased before the portal puncture for PP?
Comparing the data presented in Figure 5 (i.e., those without collaterals on conventional
angiography) to previous work (which also used conventional angiography: synthesized
in https://pubmed.ncbi.nlm.nih.gov/15908290/ or https://pubmed.ncbi.nlm.nih.gov/33068638/),
the observed poor correlation is surprising. What are the explanations by the authors? How was
alcoholic cirrhosis diagnosed? Are biopsies/liver stiffness measurements available to rule-out
INCPH/PSVD?
The latter is particularly important, as the reported prevalence of vein-vein communications in
conventional angiography seems very high for alcoholic cirrhosis – (erroneous) inclusion of
some INCPH/PSVD patients may explain this finding.
At my institution, we avoid injecting large amounts of contrast/with high pressure, assuming
that the unphysiologically high pressures/flow may affect the endothelium/sinusoids, and
thus, WHVP. Can the authors provide data on WHVP measured before and after ‘innovative
angiography?’
Minor points:
I (and most likely potential readers) cannot follow this paragraph: ‘The contrast medium was
retained in the liver parenchyma and could not enter the portal vein or the hepatic venous
collateral return. Therefore, the absence of collateral branches of the hepatic vein is an important
reason for the overestimation of WHVP and HVPG.‘ Please rephrase/explain.
Numbers should be added to the Figures.
Title: Innovative angiography: a new approach to discover more hepatic vein collaterals in
patients with cirrhotic portal hypertension
Version: 0 Date: 14 Jan 2023
Reviewer's report:
Major points:
Looking at Figure 4 panel C, it is unclear to me why there was only a small discordance
between WHVP and PP, however, there was substantial discordance between HVPG and PPG.
Since FHVP/VCIP should basically be the same, what is the explanation for this discordance?
The same applies to Figure 6, panel A. Even in Figure 5, differences in WHVP and PP seem
substantially lower than those in HVPG/PPG. How was PPG calculated? If the RAP was used,
it should be exchanged for the VCIP (or FHVP, if VCIP was not measured) – see Baveno VII
recommendations.
Moreover, since sedation/analgesia impacts pressure measurements, the regimens should be
reported. Were the regimens the same when measuring WHVP and PP, or was sedation/analgesia
added/increased before the portal puncture for PP?
Comparing the data presented in Figure 5 (i.e., those without collaterals on conventional
angiography) to previous work (which also used conventional angiography: synthesized
in https://pubmed.ncbi.nlm.nih.gov/15908290/ or https://pubmed.ncbi.nlm.nih.gov/33068638/),
the observed poor correlation is surprising. What are the explanations by the authors? How was
alcoholic cirrhosis diagnosed? Are biopsies/liver stiffness measurements available to rule-out
INCPH/PSVD?
The latter is particularly important, as the reported prevalence of vein-vein communications in
conventional angiography seems very high for alcoholic cirrhosis – (erroneous) inclusion of
some INCPH/PSVD patients may explain this finding.
At my institution, we avoid injecting large amounts of contrast/with high pressure, assuming
that the unphysiologically high pressures/flow may affect the endothelium/sinusoids, and
thus, WHVP. Can the authors provide data on WHVP measured before and after ‘innovative
angiography?’
Minor points:
I (and most likely potential readers) cannot follow this paragraph: ‘The contrast medium was
retained in the liver parenchyma and could not enter the portal vein or the hepatic venous
collateral return. Therefore, the absence of collateral branches of the hepatic vein is an important
reason for the overestimation of WHVP and HVPG.‘ Please rephrase/explain.
Numbers should be added to the Figures.
Please review this paper.
user
Title: Innovative angiography: a new approach to discover more hepatic vein collaterals in
patients with cirrhotic portal hypertension
Version: 0 Date: 14 Jan 2023
Reviewer's report:
Major points:
Looking at Figure 4 panel C, it is unclear to me why there was only a small discordance
between WHVP and PP, however, there was substantial discordance between HVPG and PPG.
Since FHVP/VCIP should basically be the same, what is the explanation for this discordance?
The same applies to Figure 6, panel A. Even in Figure 5, differences in WHVP and PP seem
substantially lower than those in HVPG/PPG. How was PPG calculated? If the RAP was used,
it should be exchanged for the VCIP (or FHVP, if VCIP was not measured) – see Baveno VII
recommendations.
Moreover, since sedation/analgesia impacts pressure measurements, the regimens should be
reported. Were the regimens the same when measuring WHVP and PP, or was sedation/analgesia
added/increased before the portal puncture for PP?
Comparing the data presented in Figure 5 (i.e., those without collaterals on conventional
angiography) to previous work (which also used conventional angiography: synthesized
in https://pubmed.ncbi.nlm.nih.gov/15908290/ or https://pubmed.ncbi.nlm.nih.gov/33068638/),
the observed poor correlation is surprising. What are the explanations by the authors? How was
alcoholic cirrhosis diagnosed? Are biopsies/liver stiffness measurements available to rule-out
INCPH/PSVD?
The latter is particularly important, as the reported prevalence of vein-vein communications in
conventional angiography seems very high for alcoholic cirrhosis – (erroneous) inclusion of
some INCPH/PSVD patients may explain this finding.
At my institution, we avoid injecting large amounts of contrast/with high pressure, assuming
that the unphysiologically high pressures/flow may affect the endothelium/sinusoids, and
thus, WHVP. Can the authors provide data on WHVP measured before and after ‘innovative
angiography?’
Minor points:
I (and most likely potential readers) cannot follow this paragraph: ‘The contrast medium was
retained in the liver parenchyma and could not enter the portal vein or the hepatic venous
collateral return. Therefore, the absence of collateral branches of the hepatic vein is an important
reason for the overestimation of WHVP and HVPG.‘ Please rephrase/explain.
Numbers should be added to the Figures.
assistant