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1.
Figure 3

Figure 3. The Many Aspects of Hypertensive Heart Disease. From: The Hypertensive Heart: An Integrated Understanding Informed by Imaging.

Hypertensive heart disease involves disparate elements, ranging aortopathy to myocardial remodeling and even peripheral energy utilization that interact to produce sequelae such as heart failure, arrhythmias and ischemic events.

Subha V. Raman. J Am Coll Cardiol. ;55(2):91-96.
2.
Figure 1:

Figure 1:. From: Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study.

Estimated proportion of women without end-stage renal disease among those with and without hypertensive disorders during pregnancy. Log-rank test, p < 0.001.

I-Kuan Wang, et al. CMAJ. 2013 February 19;185(3):207-213.
3.
Figure 6.

Figure 6. From: Chromogranin A Polymorphisms Are Associated With Hypertensive Renal Disease.

Hypothesis: Proposed mechanism of action of CHGA 3′-UTR variation on a disease trait such as hypertensive ESRD. A potential mechanism for the role of variation (+87T) in the CHGA 3′-UTR influences CHGA and hence catestatin expression, altering sympathoadrenal activity and ultimately resulting in elevated risk for hypertensive ESRD.

Rany M. Salem, et al. J Am Soc Nephrol. 2008 March;19(3):600-614.
4.
Figure 1

Figure 1. From: A consensus approach to the classification of pediatric pulmonary hypertensive vascular disease: Report from the PVRI Pediatric Taskforce, Panama 2011.

Venn diagram illustrating the heterogeneity and multifactorial elements in pediatric pulmonary hypertensive vascular disease.

Maria Jesus del Cerro, et al. Pulm Circ. 2011 Apr-Jun;1(2):286-298.
5.
Figure 13

Figure 13. From: The Burden of Cardiovascular Disease in the Elderly: Morbidity, Mortality, and Costs.

Estimated Direct and Indirect Costs in Billions of Dollars of Cardiovascular Disease and Stroke
Heart Disease category includes coronary heart disease, heart failure, stroke and part of hypertensive disease, cardiac dysrhythmias, rheumatic heart disease, cardiomyopathy, pulmonary heart disease, and other or ill-defined “heart” disease.
Source: Heart Disease and Stroke Statistics-2009 Update. Available at: www.myamericanheart.org.

Ali Yazdanyar, et al. Clin Geriatr Med. ;25(4):563-vii.
6.
Figure 3.

Figure 3. From: The @neurIST Ontology of Intracranial Aneurysms: Providing Terminological Services for an Integrated IT Infrastructure.

Part of the risk model of the @neurIST ontology exemplifying the usage of DOLCE and domain-specific relations. Displayed is the state of a patient with hypertensive disease and an existing intracranial aneurysm – the patient is in an intracranial aneurysm state. Entity type “Patient” participates in the process of “Hypertensive Disease (“dol:participant-in” is the corresponding DOLCE relation). “Hypertensive Disease” is a known risk factor for the rupture of intracranial aneurysms which is by “Hypertensive Disease” triggers “Aneurysm Rupture Disposition” with the domain specific relation “triggers”. The “Aneurysm Rupture Disposition” will manifest itself with a certain probability (“has_realization”) as “Ruptured Intracranial Aneurysm State”. The manifestation state of intracranial aneurysm has again as a “dol:participant” the type “Intracranial Aneurysm”.

Martin Boeker, et al. AMIA Annu Symp Proc. 2007;2007:56-60.
7.
Figure 1

Figure 1. From: A clinical predictor of varices and portal hypertensive gastropathy in patients with chronic liver disease.

Comparison of receiver operating characteristic curves between the varices and portal hypertensive gastropathy score and the platelet count/spleen diameter ratio for predicting of esophageal varices, gastric varices, and portal hypertensive gastropathy. VAP, varices and portal hypertensive gastropathy; Plt/S-D ratio, platelet count/spleen diameter ratio.

Yang Won Min, et al. Clin Mol Hepatol. 2012 June;18(2):178-184.
8.
Figure 1

Figure 1. From: Metalloproteinases: key and common mediators of multiple GPCRs and candidate therapeutic targets in models of hypertensive cardiac disease.

Hypertensive cardiac disease is a consequence of diverse conditions and morbidities. Conditions such as chronic stress, environmental factors, genetic predisposition and metabolic morbidities trigger responses systemically and locally (on target cardiovascular organs) which lead to excessive signaling by GPCR agonists. This translates into unchecked proteolytic activity of metalloproteinases that regulate many substrates including growth factors, cytokines and cell surface receptors. Uncontrolled cleavage of these substrates contributes to the development of hypertensive cardiac disease.

Xiang Wang, et al. Drug Discov Today Dis Models. ;9(3):e103-e108.
9.
FIGURE 1

FIGURE 1. From: Elevated circulating fibrocyte levels in patients with hypertensive heart disease.

Median values of circulating blood fibrocyte concentrations (× 106/ml) in normal controls compared to individuals with hypertensive heart disease (HHD). Panel (a) shows total fibrocytes (P < 0.0001). Panel (b) shows activated fibrocytes (P < 0.0001). Panel (c) shows CXCR4+ fibrocytes (P < 0.0001). Panel (d) shows CCR2+ fibrocytes (P < 0.0001). Panel (e) shows CCR7+ fibrocytes (P < 0.0001). Panel (f) shows CXCR4+CCR2+ fibrocytes (P < 0.001).

Ellen C. Keeley, et al. J Hypertens. 2012 September;30(9):1856-1861.
10.
Figure 3

Figure 3. Uric acid in the first trimester compared to uric acid at delivery in women who A. remained normotensive, or B. developed hypertensive disease. From: First trimester uric acid and adverse pregnancy outcomes.

Figure 3A. In women who remained normotensive, 12% of the variance of uric acid at delivery was explained by uric acid in the first trimester; B. In women who developed hypertensive disease (H=gestational hypertension, HP= preeclampsia, HU= hyperuricemic gestational hypertension, and HPU= hyperuricemic preeclampsia), 23% of the variance of uric acid at delivery was explained by uric acid in the first trimester. The closed circles represent women who developed H or HP and the open circles represent women who developed HU or HPU.

S.K. Laughon, et al. Am J Hypertens. ;24(4):489-495.
13.
Figure 1

Figure 1. From: Impact of serum uric acid on renal function and cardiovascular events in hypertensive patients treated with losartan.

Serial changes in the estimated glomerular filtration rate (eGFR) in hypertensive patients with or without chronic kidney disease.

Sadayoshi Ito, et al. Hypertens Res. 2012 August;35(8):867-873.
15.
FIGURE 2

FIGURE 2. From: Elevated circulating fibrocyte levels in patients with hypertensive heart disease.

Correlation coefficient with 95% confidence intervals of left ventricular mass index (g/m2) as assessed by cardiac MRI with blood fibrocyte concentrations (× 106/ml) in patients with hypertensive heart disease. Panel (a) shows total fibrocytes (r = 0.65, P = 0.037). Panel (b) shows activated fibrocytes (r = 0.70, P = 0.016).

Ellen C. Keeley, et al. J Hypertens. 2012 September;30(9):1856-1861.
16.
Figure 4  

Figure 4  . From: Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function.

Relation between asynchrony index (x axis) and deceleration time of early transmitral filling (E-DT, y axis). The correlations were significant for both hypertrophic cardiomyopathy (HCM, empty circles, uninterrupted regression line: y = 192 + 509x; r = 0.56, p = 0.02) and hypertensive heart disease (HT, rectangles, dashed regression line; y = 158 + 680x; r = 0.59, p<0.05).

S F De Marchi, et al. Heart. 2000 June;83(6):678-684.
17.
Figure 3  

Figure 3  . From: Relaxation in hypertrophic cardiomyopathy and hypertensive heart disease: relations between hypertrophy and diastolic function.

There was a significant correlation between left ventricular asymmetry (x axis) and the asynchrony index (y axis) (y = 0.05 + 0.23x; r = 0.49, p = 0.02), but not for the individual groups. Patients with abnormal asynchrony index did not differ from patients with normal asynchrony index in terms of left ventricular asymmetry. HCM. Hypertrophic cardiomyopathy; HT, hypertensive heart disease; N, normal.

S F De Marchi, et al. Heart. 2000 June;83(6):678-684.
18.
Fig. 2

Fig. 2. From: Progression of Chronic Kidney Disease: Adrenergic Genetic Influence on Glomerular Filtration Rate Decline in Hypertensive Nephrosclerosis.

ADRB2 variant Gly16Arg: risk/susceptibility genotype for Black hypertensive ESRD. The figure shows ADRB2 Gly16Arg diploid genotype frequency distributions between hypertensive ESRD cases and healthy controls. All subjects were African-American (by self-identification).

Yuqing Chen, et al. Am J Nephrol. 2010 July;32(1):23-30.
19.
Figure 2

Figure 2. From: Thirty-year Survival for Black and White Hypertensive Individuals in the Evans County Heart Study and the Hypertension Detection and Follow-up Program.

Survival curves for cardiovascular disease for Hypertension Detection and Follow-up Program-Georgia Site (HDFP) and Evans County Heart Study hypertensive cohort (ECHS)

Daniel T. Lackland, et al. J Am Soc Hypertens. ;2(6):448-454.
20.
Figure 1.

Figure 1. From: Improving Outcomes for Pulmonary Vascular Disease.

Pediatric pulmonary hypertensive vascular disorders often have multiple factors that contribute to the severity of pulmonary vascular disease.

Ivan M. Robbins, et al. Am J Respir Crit Care Med. 2012 May 1;185(9):1015-1020.

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