Angiographic Evaluation of Coronary Microvascular Dysfunction in Patients with Heart Failure and Preserved Ejection Fraction

Sucato, Vincenzo; Evola, Salvatore; Novo, Giuseppina; Sansone, A; Quagliana, Angelo; Andolina, Giuseppe; Assennato, Pasquale; Novo, Salvatore

doi:10.1111/micc.12223

Cited by 29 publications

(27 citation statements)

References 30 publications

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“…Coronary microvascular dysfunction (CMD), which is present in a high proportion of patients with angina and no obstructive CAD, has also been found in many patients with heart failure with preserved ejection fraction . Therefore, CMD has been suggested to be linked to diastolic dysfunction and, ultimately, heart failure . This association could be a manifestation of causality or, for example, existence of shared causal factors.…”

Section: Discussionmentioning

confidence: 99%

“…In patients with CAD (n = 40), heart failure with reduced LVEF (n = 47), and in patients with diabetes (n = 67), CMD has been shown to correlate with indices of LV diastolic dysfunction or/and high LV filling pressure . Further, a study including patients with angina, no coronary artery stenosis, and preserved LVEF showed that those with diastolic heart failure (n = 155) had a more impaired coronary microcirculation determined by angiographic indices than those without heart failure (n = 131), although the authors did not adjust for differences in cardiovascular risk factors between groups . In this present study investigating a cohort of symptomatic women with normal LVEF, the number of patients with severe diastolic function was very low.…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that CMD can cause left ventricular (LV) diastolic dysfunction and contribute to development of heart failure with preserved ejection fraction but limited data exist in support of this hypothesis . Further, it is unknown whether CMD affects LV systolic function.…”

Section: Introductionmentioning

confidence: 99%

“…5,[9][10][11][12] It has been suggested that CMD can cause left ventricular (LV) diastolic dysfunction and contribute to development of heart failure with preserved ejection fraction but limited data exist in support of this hypothesis. [13][14][15][16][17] Further, it is unknown whether CMD affects LV systolic function. Speckle tracking-derived global longitudinal strain (GLS) determined by transthoracic echocardiography can detect early LV dysfunction at rest and provides incremental information compared with traditional measures such as LV ejection fraction (LVEF).…”

Section: Introductionmentioning

confidence: 99%

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Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease

et al. 2017

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“…Diastolic dysfunction is likely an antecedent event that interacts synergistically with other remodeling events at the cellular level to foster development of HFpEF. Recently, levels of inflammatory cells in endomyocardial biopsy samples from HFpEF patients were found to positively correlate with diastolic dysfunction (69) and coronary microvascular dysfunction was detected by angiography in patients with HFpEF (70). Further support for the involvement of myocardial microvascular inflammatory endothelial activation in the etiology of HFpEF comes from a study by Franssen et al (71).…”

Section: Role Of Coronary Microvascular Inflammationmentioning

confidence: 99%

Targeting Obesity and Diabetes to Treat Heart Failure with Preserved Ejection Fraction

et al. 2017

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Heart failure with preserved ejection fraction (HFpEF) is a major unmet medical need that is characterized by the presence of multiple cardiovascular and non-cardiovascular comorbidities. Foremost among these comorbidities are obesity and diabetes, which are not only risk factors for the development of HFpEF, but worsen symptoms and outcome. Coronary microvascular inflammation with endothelial dysfunction is a common denominator among HFpEF, obesity, and diabetes that likely explains at least in part the etiology of HFpEF and its synergistic relationship with obesity and diabetes. Thus, pharmacological strategies to supplement nitric oxide and subsequent cyclic guanosine monophosphate (cGMP)—protein kinase G (PKG) signaling may have therapeutic promise. Other potential approaches include exercise and lifestyle modifications, as well as targeting endothelial cell mineralocorticoid receptors, non-coding RNAs, sodium glucose transporter 2 inhibitors, and enhancers of natriuretic peptide protective NO-independent cGMP-initiated and alternative signaling, such as LCZ696 and phosphodiesterase-9 inhibitors. Additionally, understanding the role of adipokines in HFpEF may lead to new treatments. Identifying novel drug targets based on the shared underlying microvascular disease process may improve the quality of life and lifespan of those afflicted with both HFpEF and obesity or diabetes, or even prevent its occurrence.

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Derangements in adrenergic–adipokine signalling establish a neurohormonal basis for obesity‐related heart failure with a preserved ejection fraction

Packer

2018

European J of Heart Fail

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Among patients with heart failure and a preserved ejection (HFpEF), obesity is associated with a distinct phenotype that is characterized by adiposity-driven plasma volume expansion and cardiac overfilling, which is coupled with an impairment of ventricular distensibility. These pathophysiological abnormalities may be related to the increased actions of specific adipocyte-derived signalling molecules (aldosterone, neprilysin and leptin) that work in concert with increased renal sympathetic nerve traffic and activated beta -adrenergic receptors to promote sodium retention, microvascular rarefaction, cardiac fibrosis and systemic inflammation. This interplay leads to striking activation of the mineralocorticoid receptor, possibly explaining why obese patients with heart failure are most likely to benefit from spironolactone and eplerenone in large-scale clinical trials. Additionally, adipocytes express and release neprilysin, which (by degrading endogenous natriuretic peptides) can further promote plasma volume expansion and cardiac fibrosis. Heightened neprilysin activity may explain the low circulating levels of natriuretic peptides in obesity, the accelerated breakdown of natriuretic peptides in HFpEF, and the cardiac decompression following neprilysin inhibition in HFpEF patients who are obese. Furthermore, as adipose tissue accumulates and becomes dysfunctional, its secretion of leptin promotes renal sodium retention, microvascular changes and fibrotic processes in the heart, and systemic inflammation; these effects may be mediated or potentiated by the activation of beta -adrenergic receptors. These adrenergic-adipokine interactions provide a mechanistic framework for novel therapeutic strategies to alleviate the pathophysiological abnormalities of obesity-related HFpEF. Ongoing trials are well-positioned to test this hypothesis.

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Angiographic Evaluation of Coronary Microvascular Dysfunction in Patients with Heart Failure and Preserved Ejection Fraction

Abstract: Analysis of microcirculation through angiography indices in patients with and without HFPEF has led to assess that the HFPEF population has a greater involvement of microcirculation than patients without HFPEF.

Cited by 29 publications

References 30 publications

Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease

Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease

Targeting Obesity and Diabetes to Treat Heart Failure with Preserved Ejection Fraction

Derangements in adrenergic–adipokine signalling establish a neurohormonal basis for obesity‐related heart failure with a preserved ejection fraction

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