2022
DOI: 10.1016/j.carpath.2022.107448
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Commentary on the enigma of small vessel disease in hypertrophic cardiomyopathy: is invasive assessment of microvascular resistance a novel independent predictor of prognosis?

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Cited by 7 publications
(6 citation statements)
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“…Subendocardial ischaemia is an especially important cause of chronic angina and acute coronary syndrome without obstructive coronary artery in patients with HCM. Small vessel disease has been suggested to contribute to myocardial ischaemia and coronary microvascular dysfunction in the HCM population 43 . Mechanisms that are unique to HCM include (i) increased left ventricular wall thickness and (ii) increased left ventricular intracavitary pressures due to outflow or mid‐cavitary obstruction 44 .…”
Section: Discussionmentioning
confidence: 99%
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“…Subendocardial ischaemia is an especially important cause of chronic angina and acute coronary syndrome without obstructive coronary artery in patients with HCM. Small vessel disease has been suggested to contribute to myocardial ischaemia and coronary microvascular dysfunction in the HCM population 43 . Mechanisms that are unique to HCM include (i) increased left ventricular wall thickness and (ii) increased left ventricular intracavitary pressures due to outflow or mid‐cavitary obstruction 44 .…”
Section: Discussionmentioning
confidence: 99%
“…Small vessel disease has been suggested to contribute to myocardial ischaemia and coronary microvascular dysfunction in the HCM population. 43 Mechanisms that are unique to HCM include (i) increased left ventricular wall thickness and (ii) increased left ventricular intracavitary pressures due to outflow or mid-cavitary obstruction. 44 Indeed, acute coronary syndrome without obstructive coronary artery is not an uncommon initial presentation (prevalence 9-14%) in patients with HCM.…”
Section: Potential Mechanismsmentioning
confidence: 99%
“…Myocardial fibrosis (LGE) is progressive in some patients with HCM, with impaired energetics and perfusion abnormalities postulated as possible mechanistic drivers of the fibrotic process [72]. The typical perfusion abnormality in HCM is small vessel ischemia (coronary microvascular dysfunction), which in time leads to fibrosis, although some postulate that the remodelling of the microcirculation at the arteriolar and capillary levels might also occur secondary to the fibrosis [73,74]. Moreover, there is growing evidence for the activation of fibrotic pathways occurring early in the course of the disease before hypertrophic remodelling and microvascular dysfunction and ischemia occur [75].…”
Section: Lge As Risk Stratificationmentioning
confidence: 99%
“…It should not be forgotten that treatment in HCM is not limited to septal reduction and that the prognosis and clinical course is also influenced by malignant arrhythmias and myocardial ischaemia (small vessel disease changes). 45 , 46 General treatment includes lifestyle modification (limit dehydration, decreased alcohol intake and decreased caffeine consumption. ), pharmacological (symptomatic and pathogenetic), electrophysiological ablation, invasive septal reduction therapy and implantable devices (dual chamber pacing, ICDs).…”
Section: ‘To Ablate or Operate’mentioning
confidence: 99%