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Proteomics gives a snapshot of the proteins present at a given time in a cell or an organism and might help to reveal novel diagnostic and therapeutic approaches in hypertension.

Coherence: A Novel Nonpharmacological Modality for Lowering Blood Pressure in Hypertensive Patients

A study aiming to identify urinary proteins involved in the pathogenesis of hypertension and salt sensitivity revealed different uromodulin protein levels in individuals with hypertension versus healthy individuals [ ]. Patients with higher levels of uromodulin were homozygotes for specific UMOD gene variants and displayed a decreased level of salt excretion [ ]. Metabolomics studies the metabolites resulting from biochemical degradation processes and allows conclusions to be drawn on the prevalence of such processes. Several studies highlighted distinctions in the metabolic footprint of patients with hypertension and hence the potential in its analysis e.

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Other results suggest that disorders in amino acid metabolism might play an important role in the pathogenesis of juvenile hypertension and circulating levels of uridine adenosine tetraphosphate are strongly associated with the disease [ , ]. In another study, sex-steroid pattern was significantly associated with the risk of incident hypertension [ ]. However, more clarity about the different metabolic influences is needed to translate these findings into clinical practice. With the omnipresence of new mobile technologies and connected devices, patient self-monitoring is becoming an increasingly important and promising topic across various diseases.

Despite a large number of mobile apps and devices designed to track general health and well-being and also BP specifically [ ], formal clinical research on such self-monitoring devices still seems to be limited. Some initial studies focused on patient education in patient-centered hypertension care [ , ].


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In the following chapter, we compare the content of important international guidelines regarding PHC in hypertension. In this section, we review the content of six international hypertension guidelines regarding evidence and recommendations on how to execute PHC in the management of high blood pressure. While the majority of guidelines still emphasize the importance of comprehensive PHC, only little evidence is displayed on detailed PHC.

The guidelines reviewed here are summarized in Table 4. Methodologies to detect asymptomatic organ damage in the individual patient are described. The focus for the heart is on left ventricular hypertrophy; for the vessels, it is on arterial stiffness and carotid plaque load; for kidney function, on glomerular filtration rate and the existence of established renal parenchymatous disease on proteinuria.

For the brain, the guidelines refer to silent infarctions, white matter hyperintensities, and microbleeds. Thus, all drug classes are suitable for the initiation and maintenance of antihypertensive treatment, either as monotherapy or in combination. The guideline discusses the hypotheses behind BP recommendations i. J-shaped curve theories and suggests that targeted BP will have to be revisited with additional data concerning associated organ damage and evaluating different end points left ventricular hypertrophy, new-onset microalbuminuria, renal failure, cardiovascular events, etc.

It suggests therapy stratification of antihypertensive drugs for specific conditions and organ damage types e. Monitoring of end-organ damage with bio markers e.

Historical Trends and Milestones in Hypertension Research | Hypertension

Further detail is given on the combinatory possibilities of the drug classes. The US Eighth Joint National Committee JNC8 guideline [ ] presents an evidence-based approach for the management of hypertension in adults to recommend treatment thresholds, goals, and medications. JNC8 stratifies its blood-pressure-lowering therapy recommendations based on age, ethnicity black vs. JNC8 gives eight recommendations based on systematic review of the literature. A ninth recommendation was developed by the panel members based on expert opinion to aid physicians in implementing JNC8.

It includes an algorithm summarizing recommendations 1—8 and advice on combining antihypertensive drugs. JNC8 acknowledges that recommendation 9 has not been validated with respect to achieving improved patient outcomes and there will likely be no supporting evidence from well-designed randomized controlled trials. Start one drug and then add a second drug before achieving maximum dose of the initial drug. Begin with two drugs at the same time, either as two separate pills or as a single pill combination. Continuous monitoring of BP is advised to adjust the treatment regimen until target BP is reached.

The combination of an ACEi and angiotensin receptor blocker should not be used. If an antihypertensive drug is not effective in a specific situation or has an adverse effect, it can be replaced. The Canadian Hypertension Education Program CHEP treatment guidelines [ ] provide recommendations for the indication of drug therapy, therapy goals, and detailed patient categorization according to their organ damage or comorbidities. Additional hypertension treatment categories are ischemic heart disease coronary artery disease or a recent myocardial infarction , heart failure, stroke acute and non-acute management , left ventricular hypertrophy, non-diabetic CKD, renovascular disease, and diabetes mellitus.

A thiazide-like diuretic chlorthalidone, indapamide can be selected instead of a CCB if the patients present with edema, intolerance, heart failure, or a high risk of heart failure.

source Alternatively, a thiazide-like diuretic can be used. Patients with stage 1 hypertension should start with lifestyle modification and treatment with a thiazide diuretic should be considered. The next treatment step involves using the highest tolerated dose or adding another antihypertensive. In the American Society of Hypertension and International Society of Hypertension clinical practice guidelines, the BP targets are defined according to age and comorbidities [ ]. Expectations regarding potential benefits for patients, clinicians, and health-care systems are as follows:.

Although some therapy guidance is provided by the guidelines, the method of selection for antihypertensive therapy is largely empirical [ ] and an individual cardiovascular and renal event risk assessment is yet not possible. In the various guidelines, different approaches have been taken to stratify patients and integrate BP with either age and ethnicity or other risk factors. Some guidelines e. This approach is based on the finding that BP reduction is not considered to be the only mechanism acting to reduce cardiovascular risk, as BP-independent, probably class-specific effects seem to contribute to the effects of risk reduction with BP-lowering drugs.

In a recent meta-analysis, the evidence of risk reduction for congestive heart disease and heart failure, and particularly mortality, was found with some drug classes only [ ]. There are efforts to understand the molecular underpinnings of BP regulation. The hope is that this will improve the prediction of cardiovascular susceptibility and thus could in the future offer insight into personalized hypertension treatment. As hypertension is a difficult phenotype to access, owing to its variability and susceptibility to other environmental factors and physiological pathways, another approach could be to search for predictors of antihypertensive drug responses.

If robust predictors of BP response are available, therapy stratification will be feasible, which could facilitate treatment success. The available data on genetic markers have been promising in terms of defining genetic determinants of response to antihypertensive drugs. However, no studies to date have been sufficiently powered with an effect size large enough to allow genetic markers of antihypertensive drug responses to be included in the guidelines to inform individualized antihypertensive treatment decisions. Despite a lack of pharmacogenomics for personalized antihypertension treatment-guided approaches, Clinical Pharmacogenetics Implementation Consortium guidelines [ ] are available for other cardiovascular drugs i.

To overcome the challenges small sample sizes in available studies with well-characterized BP responses and genetic data, replication of genomic signals in independent cohorts, identification of the biological basis for the genetic association, etc. In addition, the US President Barack Obama has announced a research initiative that aims to accelerate progress toward a new era of precision medicine [ ], www.

Despite advances in research and technologies, the PHC concept is still new for a number of physicians and it remains unclear how quickly the adoption of PHC into routine practice will occur. There is wide variation in inter-individual responses to anticoagulants, such as clopidogrel, as well as to statin therapy with underlying genetic differences assumed to be responsible [ , ].

In fact, of patients with an acute myocardial infarction treated with clopidogrel, those carrying CYP2C19 loss-of-function alleles had a higher rate of subsequent cardiovascular events than non-carriers of that allele [ ]. Genetic screening to guide selection of anticoagulation and lipid-lowering therapy has been limited to date, because solid clinical data to support its use are not yet available [ , , ].

However, it is believed that the formal integration of genetic testing to optimize warfarin dosage would reduce over- or under-coagulation of patients. In order to investigate the current use and evolution of genetic testing in clinical practice, interviews with cardiologists in the USA and Germany have recently been conducted.

In a substudy of a recently published analysis [ ], we interviewed 39 cardiologists in private practices, community hospitals, and academic centers in the USA and Germany about their use of genetic testing for diagnosis and treatment, and treatment guidance. Physicians were initially asked about how frequently they order genetic genotyping tests for cardiovascular risk factors in patients with heart failure: i before prescribing warfarin or clopidogrel and ii before prescribing statin drugs or hydralazine. They were also asked iii how frequently they order genetic tests to diagnose or assess the risk of long QT syndrome and various cardiomyopathies or to monitor transplant rejection in heart-transplant patients.

In conclusion, the cardiologists were asked iv how they expect the use of personalized medicine tests to change in the area of heart failure and hypertension. The results of our interviews are summarized in Table 5 and Figure 3. Only one US cardiologist routinely ordered genotyping tests to determine patient response to clopidogrel or warfarin. The majority of interviewees indicated that they never or rarely ordered these tests in cases of non-response to treatment, with numbers being close to equal in the USA and Germany.

Functional thrombocyte tests were ordered as they were reimbursed.

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In the case of statins, only one cardiologist in the USA and two in Germany ordered genetic tests frequently for all patients to assess responsiveness to statin drugs or for inheritance of familial hypercholesterolemia. Limited clinical benefit, cost, and reimbursement were mentioned as the main reasons for not using these tests. Although patients with cardiomyopathies, such as long QT syndrome, and transplant patients, were rare compared with anticoagulation patients, physicians seem to be aware of the genetic tests that have been developed for those conditions.


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Physicians in private practice often indicated that they referred their patients to an academic center for specialized evaluation. Despite the fact that currently most cardiologists barely use PHC tests, most believe that the use of such tests will increase over the next decade. Despite the fact that the concept of personalized medicine has been discussed in cardiology for over a decade, our study has confirmed that there is still no regular use of genetic tests for pharmacogenomic-guided treatment in cardiovascular disease [ ].

Our study has shown that only one to three cardiologists out of 39 ordered genetic tests on a regular basis before prescribing anticoagulation or statins. One reason for the limited use of genetic testing for pharmacogenomics in cardiology seems to be a lack of sufficient clinical evidence. Physicians often indicate that there is no adequate benefit to be gained from these tests, which has been mentioned in earlier studies [ ]. Even though newer studies have demonstrated the value of genetic testing e.

Another reason stated by the physicians is the cost of these tests or the lack of reimbursement. Both reasons highlight little awareness of the value of genetic testing in terms of economic benefits, which would equal clinical utility and cost-effectiveness [ ]. This indicates that more studies are needed to generate clinical evidence and proof of economic value for genetic testing in patients with cardiovascular diseases. Despite being a secondary form of hypertension, its prevalence is associated with the existence of chronic hypertension in women.

Hypertension is the most common complication of pregnancy [ ]. Although many pregnant women with high BP have healthy babies, hypertension during pregnancy can be dangerous for both mother and fetus. Hypertensive disorders of pregnancy can be classified as follows: a chronic hypertension high BP that either precedes pregnancy, is diagnosed within the first 20 weeks of pregnancy, or does not resolve by the week postpartum checkup , b gestational hypertension transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy , c preeclampsia-eclampsia, or d preeclampsia superimposed on chronic hypertension [ ].

Effects of high BP range from mild to very severe, with serious cases causing maternal and fetal harm. Preeclampsia and eclampsia, in particular, can be life-threatening for mother and baby. It is associated with placental dysfunction and can result in adverse outcomes for mother and child. Maternal adverse outcomes include eclampsia seizures , HELLP syndrome hemolysis, elevated liver enzymes, low platelets , early delivery, placental abruption, renal failure, and death [ — ]. Adverse outcomes for the child include intrauterine growth restriction IUGR , intraventricular hemorrhage, necrotizing enterocolitis, and perinatal death.

The clinical features of preeclampsia are often variable and non-specific.