Increased Extracellular Volume and Altered Mechanics Are Associated With LVH in Hypertensive Heart Disease, Not Hypertension Alone

Kuruvilla, Sujith; Janardhanan, Rajesh; Antkowiak, Patrick F.; Keeley, Ellen C.; Adenaw, Nebiyu; Brooks, Jeremy; Epstein, Frederick H.; Kramer, Christopher M.; Salerno, Michael

doi:10.1016/j.jcmg.2014.09.020

Cited by 146 publications

(118 citation statements)

References 29 publications

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“…The authors demonstrate early native T1 changes. This finding, in part, agrees with previous HCM studies, one measuring circulating peripheral biomarkers of fibrosis (presumably myocardial), 10 and another indicating elevations in myocardial ECV associated with increased pro-brain natriuretic peptide levels and decreased mitral annular E′ velocities.11 The authors did not find these changes in HHD-also concordant with 2 studies where native T1 and ECV only increased in the setting of frank left ventricular hypertrophy, 12,13 suggesting that cellular hypertrophy may develop without disproportionate fibrosis in early HHD yielding normal ECV. But if fibrosis seems early in HCM, why did native T1 increase alone, without an associated ECV increase?…”

supporting

confidence: 86%

“…11 The authors did not find these changes in HHD-also concordant with 2 studies where native T1 and ECV only increased in the setting of frank left ventricular hypertrophy, 12,13 suggesting that cellular hypertrophy may develop without disproportionate fibrosis in early HHD yielding normal ECV. But if fibrosis seems early in HCM, why did native T1 increase alone, without an associated ECV increase?…”

mentioning

confidence: 62%

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Exploiting Differences in Myocardial Compartments With Native T1 and Extracellular Volume Fraction for the Diagnosis of Hypertrophic Cardiomyopathy

Schelbert

Moon

2015

Circ: Cardiovascular Imaging

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. At present, establishing native T1 reference ranges is needed for each particular scanner and software version because small variations in T1-mapping methodology can exert significant influence on normal reference ranges. 6 Native T1 decreases with some diseases (fat infiltration and iron overload) and increases in others (fibrosis, edema, and amyloid). In myocardial fibrosis, the native T1 elevation is likely from the interstitial compartment rather than cardiomyocyte compartment, but not definitively known.In contradistinction to native T1, ECV detects diseases limited to the interstitium (including myocardial vasculature). ECV exploits the extracellular nature of gadolinium contrast agents. The concentration of contrast in myocardium relative to the concentration in plasma (not whole blood) is a direct measure of the interstitial space after equilibration, as long as contrast agents are not protein-bound. The relative concentrations are derived from the change in relaxivity (ie, 1/T1) for myocardium and whole blood before and after contrast administration and then multiplying the resultant partition coefficient by (1 -hematocrit). The latter term accounts for the displacement of plasma by erythrocytes and enables computation of plasma contrast concentration from the whole-blood measurement from regions of interest measured from the T1 images.ECV and T1 have their respective limitations. The signal to noise ratio of the biological signal to be detected may be massive in some diseases (iron, Fabry, and amyloid) but smaller in diffuse fibrosis. Small signals are intrinsically harder to detect and more prone to potential biases and difficulties with quality control, particularly between centers. There is some evidence that measurement errors are lower at 1.5T than 3T and lower for ECV compared with native T1. 8 Because the ECV and the partition coefficient are ratios, some systematic T1 biases may cancel. However, ECV requires precise T1 measurement over a broader range of values and relies on a second measurement system for the hematocrit (Coulter counter), another potential source of error. ECV also varies slightly with contrast concentration possibly from water exchange effects in and out of cells. Therefore, variations in gadolinium contrast concentration (which relates to choice of contrast timing and dose) can yield slight differences in ECV values, for example, if double-dose or single-dose contrast is used or if time intervals between contrast bolus and post contrast T1 measures vary significantly.9 Both T1 and ECV can be prone to partial volume error from adjacent tissues (eg, blood) and off resonance, so care must be taken in their measurement.What might occur in myocardial compartments with HCM, particularly early HCM? The authors demonstrate early native T1 changes. This finding, in part, agrees with previous HCM studies, one measuring circulating peripheral biomarkers of fibrosis (presumably myocardial), 10 and another indicating elevations in myocardial ECV associated with increased pro-brain natr...

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supporting

confidence: 86%

mentioning

confidence: 62%

Exploiting Differences in Myocardial Compartments With Native T1 and Extracellular Volume Fraction for the Diagnosis of Hypertrophic Cardiomyopathy

Schelbert

Moon

2015

Circ: Cardiovascular Imaging

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“…In SA, by contrast, it might conceivably relate to ultrastructural changes in the LV wall brought about by a profibrotic state. 16 However, these data should be interpreted with some caveats borne in mind. Certainly, the addition of left atrial volume or linear dimension and inclusion of pulmonary artery systolic pressure would have provided support for significant diastolic dysfunction, as is suggested in recent guidelines for diastolic function analysis.…”

Section: See Article By Cesari Et Almentioning

confidence: 98%

Cardiac Structure and Function in Hyperaldosteronism

Parker

Aurigemma

2016

Circ: Cardiovascular Imaging

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C hronic activation of the renin-angiotensin-aldosterone system is known to be associated with cardiovascular injury. Primary aldosteronism (PA), either from bilateral adrenal hyperplasia or an aldosterone-secreting tumor, is one of the principal causes of secondary hypertension. The combined vascular resistance and sodium retention lead to increased afterload and result in increased left ventricular (LV) wall thickness, most often with minimal change in LV diameter. However, left ventricular hypertrophy (LVH) is more common and more pronounced in PA than in either essential hypertension 2 or in other secondary forms of hypertension, such as pheochromocytoma or Cushing disease.3 Tissue Doppler studies have also demonstrated a higher prevalence of subclinical abnormalities of systolic and diastolic dysfunction in patients with this condition compared with age-matched patients with essential hypertension. 4 See Article by Cesari et alThe hormonal effects of aldosterone seem to amplify the hemodynamic effects of aldosterone-related hypertension by changing the composition of the cardiac extracellular matrix, 5 a pathophysiology that has proven to be an important therapeutic target. 6 Secondary aldosteronism (SA), commonly associated with cirrhosis of the liver but also present in renal vascular disease, often results in higher circulating levels of aldosterone than is seen in PA but is not necessarily associated with hypertension. Specifically in cirrhosis, blood pressure and systemic vascular resistance are low because of obligatory splanchnic dilatation. The cardiac effects of SA in cirrhosis including LV remodeling, proarrhythmia, and reduced contractile reserve, are collectively referred to as cirrhotic cardiomyopathy. 7 The principal hemodynamic finding is that of a high-output state, with higher systolic performance and lower peripheral vascular resistance than healthy controls, but the usual anatomic finding is a normal LV cavity diameter with increased LV wall thickness, 8,9 similar to that seen in PA. There is also echocardiographic evidence of diastolic dysfunction in patients with cirrhosis; most series report decreased early mitral inflow velocities and decreased left atrial contribution to ventricular filling. 8,9 Animal models of PA and SA have demonstrated that myocardial fibrosis occurs in both forms of hyperaldosteronism, whether or not hypertension is present. 10With this background, we will examine the interesting article by Cesari et al 11 in this issue of Circulation: Cardiovascular Imaging. Their purpose was to investigate whether PA and SA, which both feature high aldosterone levels, but different hemodynamic loads and plasma renin levels, are associated with different echocardiographic phenotypes. Accordingly they studied a remarkably large number of patients with PA, collected over 23 years from 1992 to 2015, and contrasted their LV structure and function with a large group of patients with SA, primarily because of liver cirrhosis, during the same time period. By contrasting echo findings i...

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“…Kuruvilla et al 15 also demonstrated a correlation with regional systolic function (peak circumferential strain and early diastolic strain rate). This work extends observations made with CMR tagging and speckle-tracking strain imaging which has shown that some hypertensives with LVH and normal ejection fraction have abnormalities of regional function, 17,18 though such regional strain abnormalities are more likely to be observed with more severe hypertension.…”

mentioning

confidence: 89%

“…Multiple studies have now analyzed changes in native T1 and ECV in hypertension and LVH. 15,16 Kuruvilla et al 15 were the first to demonstrate the increased native T1 and ECV in hypertensive heart disease patients with LVH. The study by Treibel et al 16 similarly showed increased ECV in patients with hypertensive LVH.…”

mentioning

confidence: 99%