Hypertension, Microvascular Pathology, and Prognosis After an Acute Myocardial Infarction

Carrick, David; Haig, Caroline; Maznyczka, Annette; Carberry, Jaclyn; Mangion, Kenneth; Ahmed, Nadeem; May, Vannesa Teng Yue; McEntegart, Margaret; Petrie, Mark C.; Eteiba, Hany; Lindsay, Mitchell; Hood, Stuart; Watkins, Stuart; Davie, Andrew; Mahrous, Ahmed; Mordi, Ify; Ford, Ian; Radjenovic, Aleksandra; Welsh, Paul; Sattar, Naveed; Wetherall, Kirsty; Oldroyd, Keith G.; Berry, Colin

doi:10.1161/hypertensionaha.117.10786

Cited by 39 publications

(33 citation statements)

References 51 publications

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“…A growing body of evidence suggests that impaired microvascular blood flow may be a common contributor to most heart diseases leading to HF. For instance, impaired microvascular blood flow has been found in ischemic heart disease (non-infarcted areas; Mygind et al, 2016 ), idiopathic dilated cardiomyopathy ( van den Heuvel et al, 2000 ; Roura and Bayes-Genis, 2009 ), hypertension ( Carrick et al, 2018 ), and diabetic cardiomyopathy ( Kibel et al, 2017 ; Sara et al, 2019 ). Impaired microvascular blood flow may also be a major contributor to HFpEF ( Srivaratharajah et al, 2016 ; Dryer et al, 2018 ), for which there is no effective treatment at present.…”

Section: Discussionmentioning

confidence: 99%

BNP as a New Biomarker of Cardiac Thyroid Hormone Function

et al. 2020

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Background: Cardiac re-expression of fetal genes in patients with heart failure (HF) suggests the presence of low cardiac tissue thyroid hormone (TH) function. However, serum concentrations of T3 and T4 are often normal or subclinically low, necessitating an alternative serum biomarker for low cardiac TH function to guide treatment of these patients. The clinical literature suggests that serum Brain Natriuretic Peptide (BNP) levels are inversely associated with serum triiodo-L-thyronine (T3) levels. The objective of this study was to investigate BNP as a potential serum biomarker for TH function in the heart. Methods: Two animal models of thyroid hormone deficiency: (1) 8-weeks of propyl thiouracil-induced hypothyroidism (Hypo) in adult female rats were subsequently treated with oral T3 (10 µg/kg/d) for 3, 6, or 14 days; (2) HF induced by coronary artery ligation (myocardial infarction, MI) in adult female rats was treated daily with low dose oral T3 (5 µg/kg/d) for 8 or 16 wks. Results: Six days of T3 treatment of Hypo rats normalized most cardiac functional parameters. Serum levels of BNP increased 5-fold in Hypo rats, while T3 treatment normalized BNP by day 14, showing a significant inverse relationship between serum BNP and free or total T3 concentrations. Myocardial BNP mRNA was increased 2.5fold in Hypo rats and its expression was decreased to normal values by 14 days of T3 treatment. Measurements of hemodynamic function showed significant dysfunction in MI rats after 16 weeks, with serum BNP increased by 4.5-fold and serum free and total T3 decreased significantly. Treatment with T3 decreased serum BNP while increasing total T3 indicating an inverse correlation between these two biologic factors (r 2 = 0.676, p < 0.001). Myocardial BNP mRNA was increased 5-fold in MI rats which was significantly decreased by T3 over 8 to 16 week treatment periods. Conclusions: Results from the two models of TH dysfunction confirmed an inverse relationship between tissue and serum T3 and BNP, such that the reduction in serum BNP could potentially be utilized to monitor efficacy and dosing of T3 treatment. Thus, serum BNP may serve as a reliable biomarker for cardiac TH function.

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Section: Discussionmentioning

confidence: 99%

BNP as a New Biomarker of Cardiac Thyroid Hormone Function

et al. 2020

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“…The excess risk associated with arterial hypertension ranged from 7% to 70% 6,18,20,21 . More common microvascular injury and myocardial haemorrhage contribute to the excess HF risk in patients with arterial hypertension 35 . Furthermore, higher neurohormonal activation and more common LV remodelling was described in hypertensive patients after MI 36 …”

Section: Clinical Risk Factorsmentioning

confidence: 99%

Heart failure after myocardial infarction: incidence and predictors

et al. 2020

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Aims The aim of the present paper was to provide an up-to-date view on epidemiology and risk factors of heart failure (HF) development after myocardial infarction. Methods and results Based on literature review, several clinical risk factors and biochemical, genetic, and imaging biomarkers were identified to predict the risk of HF development after myocardial infarction. Conclusions Heart failure is still a frequent complication of myocardial infarction. Timely identification of subjects at risk for HF development using a multimodality approach, and early initiation of guideline-directed HF therapy in these patients, can decrease the HF burden.

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“…Hypertension is associated with endothelial dysfunction and is a strong negative prognostic indicator after STEMI [ 79 – 81 ]. However, studies utilizing both CMR and invasive coronary physiology have been unable to demonstrate significant association between pre-existing hypertension and microvascular dysfunction following acute MI [ 79 , 82 ].…”

Section: Cardiovascular Risk Factorsmentioning

confidence: 99%

Predictors of Microvascular Reperfusion After Myocardial Infarction

et al. 2021

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Purpose of Review In acute ST-segment elevation myocardial infarction (STEMI), successful restoration of blood flow in the infarct-related coronary artery may not secure effective myocardial reperfusion. The mortality and morbidity associated with acute MI remain significant. Microvascular obstruction (MVO) represents failed microvascular reperfusion. MVO is under-recognized, independently associated with adverse cardiac prognosis and represents an unmet therapeutic need. Recent Findings Multiple factors including clinical presentation, patient characteristics, biochemical markers, and imaging parameters are associated with MVO after MI. Summary Impaired microvascular reperfusion is common following percutaneous coronary intervention (PCI). New knowledge about disease mechanisms underpins precision medicine with individualized risk assessment, investigation, and stratified therapy. To date, there are no evidence-based therapies to prevent or treat MVO post-MI. Identifying novel therapy for MVO is the next frontier.

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Hypertension, Microvascular Pathology, and Prognosis After an Acute Myocardial Infarction

Abstract: Supplemental Digital Content is available in the text.

Cited by 39 publications

References 51 publications

BNP as a New Biomarker of Cardiac Thyroid Hormone Function

BNP as a New Biomarker of Cardiac Thyroid Hormone Function

Heart failure after myocardial infarction: incidence and predictors

Predictors of Microvascular Reperfusion After Myocardial Infarction

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