Cardiac markers: Role in the pathogenesis of arterial hypertension

Table 1 Role of creatine kinase, creatine kinase-MB, cardiac troponin I, and lipoprotein (a) in the pathogenesis of arterial hypertension

Ref.	Cardiac markers	The main finding of cardiac markers in arterial hypertension
Brewster et al[11], 2006	Creatine kinase	Creatine kinase was independently associated with blood pressure, with an increase in systolic and diastolic pressure, respectively
Emokpae et al[12], 2017	Creatinine kinase-MB	The mean creatinine kinase-MB activity of the female hypertensive subjects was significantly higher than the males
McEvoy et al[13], 2015	High-sensitive cardiac troponin T	In an ambulatory population with no history of cardiovascular disease, high-sensitive cardiac troponin T was associated with incident hypertension and risk of left ventricular hypertrophy
Emokpae et al[12], 2015	Cardiac troponin I	The mean cardiac troponin I of the female hypertensive subjects was significantly higher than the males
Kim et al[14], 2022	Cardiac troponin I	Reported the elevated cardiac troponin I in the crisis of hypertensive patients which could provide useful prognostic information and permit the early identification of patients with an increased risk of death
Stefanie et al[15], 2015	High-sensitivity cardiac troponin I	The study concluded that an independent relation was found between high-sensitivity cardiac troponin I with systolic blood pressure as well as left ventricular hypertrophy
Sato et al[16], 2011	High-sensitivity cardiac troponin T	The high-sensitive cardiac troponin T was 78% of patients presenting with treated essential hypertension and independently correlated with age, renal function, and electrocardiogram voltage of hypertrophy
Afonso et al[18], 2011	Cardiac troponin I	Observed a disturbingly high incidence of mortality in individuals presenting with a hypertensive emergency, although neither the presence nor the extent of cardiac troponin I release was associated with greater odds of death
Acosta et al[19], 2020	Troponin	About one-third of patients with the hypertensive crisis have detectable troponin. Still, among these patients, less than half have troponin levels consistent with myocardial injury, and the majority of these patients have minimal changes in serial troponin
Tehrani et al[17], 2019	High-sensitive cardiac troponin T	An increase in high-sensitive cardiac troponin T over time is associated with a higher risk of cardiovascular disease even when the blood pressure is stable or decreases over time
Liu et al[22], 2021	Lipoprotein (a)	Elevated lipoprotein (a) was associated with an increased risk of A cerebrovascular events in stable coronary artery disease patients with hypertension. Moreover, the coexistence of high lipoprotein (a) concentrations and hypertension greatly worsened the clinical prognosis in patients with coronary artery disease, which may suggest a prognostic correlation between lipoprotein (a) and hypertension
Gazzaruso et al[23], 1996	Lipoprotein (a) levels and apo (a) isoforms	High lipoprotein (a) levels and apolp (a) isoforms of low molecular weight are strongly associated with a family history of coronary heart disease in hypertensives. The quantification of lipoprotein (a) levels and the characterization of apo (a) phenotypes may be used for the assessment of familial predisposition to coronary heart disease in hypertensives
Catalano et al[24], 1998	Lipoprotein (a)	Higher plasma concentrations of lipoprotein (a), albeit within the normal range, could be an independent risk factor for atherosclerosis and could contribute to increasing the incidence of cardiovascular disease in people with essential arterial hypertension.
Ghorbani et al[25], 2013	Lipoprotein (a)	There was a significant correlation between serum lipoprotein (a) and age or duration of high blood pressure
Antonicelli et al[26], 2001	Lipoprotein (a)	The study found a significant correlation was found between lipoprotein (a) levels and the night-time systolic and diastolic pressures as well as with the mean night-time fall in systolic and diastolic blood pressures
Drgan et al[27], 2011	Lipoprotein (a)	Lipoprotein (a) was significantly higher in the hypertension group than in the hypertension group and then in the control group
Sechi et al[28], 1997	Lipoprotein (a)	Reported that lipoprotein (a) levels, as well as apolipoprotein (a) phenotype, have also been shown to be related to target organ damage in patients with essential hypertension, with a higher frequency of the low molecular weight apo (a) phenotype in patients with increasing severity of target organ damage
Ward et al[29], 2021	Lipoprotein (a)	Authors suggested that in approximately 30% of the patients in this risk, lipoprotein (a) level is elevated in the hypertensive cohort and measurement of lipoprotein (a) could be useful in risk stratification
Woo et al[31], 1991	Lipoprotein (a)	The study showed a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolp (a)-I concentration to be independent risk factors for all strokes

Table 2 Role of osteopontin, extracellular matrix, and C-reactive protein in the pathogenesis of arterial hypertension

Ref.	Cardiac markers	The main finding of cardiac markers in arterial hypertension
Caesar et al[32], 2016	Osteopontin expression	The study found that hypertension-induced elevated in osteopontin expression was inhibited in transgenic smooth muscle cell-specific catalase overexpressing (TgSMC-Cat) mice
Yang et al[34], 2020	Osteopontin	Circulating osteopontin was an independent risk factor for both left ventricular hypertrophy and left ventricular diastolic dysfunction in essential hypertensive patients
Caesar et al[35],	Osteopontin	Osteopontin is upregulated with mechanical strain in smooth muscle cells and the aorta with hypertension through hydrogen peroxide
Bellan et al[36], 2021	Osteopontin	Osteopontin was significantly associated with pulmonary arterial hypertension among patients with connective tissue diseases
Cai et al[39], 2021	Extracellular ma-tri	Extracellular matrix remodeling in the component profiles, mechanical properties, degradation processes, and degraded fragment production leads to subsequent vascular wall structural and functional remodeling and results in hypertension
Smith et al[43], 2005	C-reactive protein	C-reactive protein concentrations are linked with hypertension, and pulse pressure, but adjustment for life course confounding and the Mendelian randomization approach suggests that higher C-reactive protein levels do not lead to higher blood pressure
Hage et al[44], 2013	C-reactive protein	Explained the role of C-reactive protein in hypertensive individuals which is linked with vascular stiffness, atherosclerosis and the development of end-organ damage and cardiovascular events
Sesso et al[45], 2003	C-reactive protein	C-reactive protein levels are connected with future development of hypertension, which suggests that hypertension is in part an inflammatory disorder
Lakoski et al[46], 2005	C-reactive protein	The study confirms the existence of an independent association between hypertension and inflammation in both men and women. Ethnic group differences were evident, with the strongest association observed in Chinese participants and no difference in C-reactive protein levels by hypertension status in Hispanics
Pan et al[47], 2019	High-sensitivity C-reactive protein	High-sensitivity C-reactive protein is prevalent in Yi people and does not support high-sensitivity C-reactive protein as a risk factor for prehypertension or hypertension
Shao-Yuan et al[49], 2013	C-reactive protein	The concentration of C-reactive protein was associated with systolic pressure and pulse pressure, but not with diastolic blood pressure
Van et al[50], 2022	C-reactive protein	The association between C-reactive protein and hypertension among Ghanaian migrants and urban-Ghanaian women, however, was largely explained by conventional risk factors. Thus, prevention of conventional risk factors, in particular obesity, may help to reduce the potentially low-grade inflammatory mechanism underlying hypertension

Table 3 Role of matrix metalloproteinases, tissue inhibitors of metalloproteinases, N-terminal pro-B-type natriuretic peptide, plasma renin activity levels, and dynorphin in the pathogenesis of arterial hypertension

Ref.	Cardiac markers	The main finding of cardiac markers in arterial hypertension
Prado et al[52], 2021	Matrix metalloproteinase activity	Imbalanced vascular matrix metalloproteinase activity promotes vascular dysfunction and a variety of structural alterations, resulting in vascular remodeling in hypertension
Flamant et al[53], 2007	Matrix metalloproteinase-9 activity	The onset of angiotensin II-induced hypertension is accompanied by increased matrix metalloproteinase-9 activity in conductance vessels; absence of matrix metalloproteinase-9 activity results in vessel stiffness and increased pulse pressure; and matrix metalloproteinase-9 activation is associated with a beneficial role early on in hypertension by preserving vessel compliance and alleviating blood pressure increase
Hopps et al[54], 2017	Matrix metalloproteinases and tissue inhibitors of metalloproteinases	The authors believe that in clinical practice a strategic antihypertensive therapy directed to the matrix metalloproteinase profile may be useful to decrease the risk of cardiovascular complications
Valente et al[55], 2020	Matrix metalloproteinase-9 concentrations	Matrix metalloproteinase-9 concentrations are significantly higher in the hypertensive crisis groups (urgency and emergency) compared to the control groups. Therefore, matrix metalloproteinase-9 may be a biomarker or mediator of pathophysiologic pathways in cases of acute elevations of blood pressure
Kuliczkowski et al[56], 2019	Tissue inhibitors of metalloproteinases-4, matrix metalloproteinase-2	Data showed that patients with coronary artery disease presented higher tissue inhibitors of metalloproteinase-4 and lower matrix metalloproteinase-2 concentrations regardless of hypertension and diabetes mellitus.
Tayebjee et al[57], 2004	Matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1	Increased circulating matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1 at baseline in patients with hypertension could reflect an increased deposition and retention of type I collagen at the expense of other components of extracellular matrix within the cardiac and vascular extracellular matrix
Robert et al[58], 1997	Matrix metalloproteinases	Observations suggest that depression of the degradative pathway is partly responsible for age-associated fibrosis. Thus, matrix metalloproteinase has differing involvements in the cardiac remodeling associated with hypertension or aging
Marchesi et al[61], 2012	Matrix metalloproteinase-2, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1	Suggested that matrix metalloproteinase-2, matrix metalloproteinas-9 as well as tissue inhibitor of metalloproteinases-1 could have a role as biomarkers of cardiovascular remodeling in hypertension patients
Nakatsu et al[64], 2007	Plasma B-type natriuretic peptide	Hypertensive patients with abnormal diurnal blood pressure variation patterns (non-dippers, extreme dippers, and risers) showed higher plasma B-type natriuretic peptide levels than those with normal circadian blood pressure variation (dippers)
Seven et al[65], 2015	N-terminal pro-B-type natriuretic peptide	Elevated serum concentrations of N-terminal pro-B-type natriuretic peptide are associated with prevalent hypertension whereas lower concentrations associate with incident hypertension
Freitag et al[66], 2003	Plasma brain natriuretic peptide	Higher plasma brain natriuretic peptide levels were associated with an increased risk of blood pressure progression in men but not women
Brunner et al[69], 1972	High plasma renin activity	Essential hypertension would appear to show that individuals with low plasma renin activity had a significantly lower incidence of myocardial infarction and stroke over about 10 years of observation compared to individuals with normal or high plasma renin activity
Sever et al[70], 2012	Plasma renin activity levels	Elevated plasma renin activity levels in a hypertensive population with no pre-existing cardiovascular disease do not indicate the future occurrence of cardiovascular events
Haber et al[71], 1979	Renin	Renin is crucial for regulating blood pressure in the salt- or volume-depleted condition and is in charge of the early stages of renovascular hypertension
Laragh et al[74], 2011	Plasma renin activity	Plasma renin activity testing can be used to guide the commencement, addition, or subtraction of anti-sodium-volume dependent or anti-renin-angiotensin antihypertensive drug types in hypertensive patients
Fontana et al[78], 1993	Dynorphin	Dynorphin modulates sympathetic activity via stimulation of atrial natriuretic factor which can reduce BP in hypertensive subjects
McConnaughey et al[79], 1992	Dynorphin	Findings imply that alterations in the opioid system's hippocampus receptors may be important for the main blood pressure-control mechanism
Wang et al[80], 1994	Dynorphin-A (1-8)	Dynorphin-A (1-8) injected into the hippocampal formation causes a significant drop in blood pressure in conscious hypertensive and normotensive rats, but not heart rate