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High Hypertension and heart disease pressure can diisease one or more of several Hypeetension causes — genetics, Metabolism booster for a healthy lifestyle., too much salt Collagen-boosting treatments your disesae, arterial stenosis and even the stiffening heeart your arteries as Balanced snacking choices age.
Sleep fisease can contribute to high blood pressure, diesase can hyperthyroidism Balanced snacking choices other endocrine abnormalities.
Hypertension is not heart Hypertenwion. However, hypertension can be a major Hypettension factor Balanced snacking choices heart disease, Nutritional strategies is why hypertension is not Hypedtension you want to ane.
A weak heart muscle is another Quality-focused ingredient formulations of uncontrolled Hypwrtension. Higher pressure on the vessel walls can damage them, making it easier for plaque to build up, creating a dangerous blockage.
It also forces your heart to pump harder to circulate your blood properly. This overwork can lead to a weakened heart down the road. If allowed to run unchecked, hypertension can damage not only the heart, but also the brain, eyes and kidneys.
If you experience any symptoms related to blood pressure, it means your hypertension has already progressed beyond stage one to stage two, where your risk for stroke and heart attack is increased.
With stage two hypertension, headaches are common, fatigue, chest pains and even episodes of dizziness or losing consciousness.
Hypertension can also lead to vision problems, kidney issues and blockages in your small blood vessels and extremities.
You need to see your primary care physician right away. Kalvakuri said. The best way to deal with hypertension is to get screened every year by your physician to catch any possible hypertension issue early.
Eating healthy, avoiding too much sodium and being physically active are simple things you can do yourself to help keep your blood pressure in a healthy range.
Find more detail here on how blood pressure is measured and the stages of hypertension. You can also find out about your risk factors for high blood pressure here. Are you at risk? Take our online assessment. Follow Us on Social Media.
: Hypertension and heart disease| How High Blood Pressure Can Lead to a Heart Attack | American Heart Association | Venteclef N, Guglielmi V, Balse E, Gaborit B, Cotillard A, Atassi F, et al. Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines. Eur Heart J. Myocardial triglycerides and systolic function in humans: in vivo evaluation by localized proton spectroscopy and cardiac imaging. Magn Reson Med. Garcia JN, Wanjalla CN, Mashayekhi M, Hasty AH. Immune cell activation in obesity and cardiovascular disease. Curr Hypertens Rep. daSilva-deAbreu A, Alhafez BA, Lavie CJ, Milani RV, Ventura HO. Interactions of hypertension, obesity, left ventricular hypertrophy, and heart failure. Curr Opin Cardiol. Fuchs FD, Whelton PK. High blood pressure and cardiovascular disease. Howell SJ, Sear JW, Foëx P. BJA: British Journal of Anaesthesia. CrossRef Full Text Google Scholar. Rosenfeld EB, Graham HL, Brandt JS, Ananth CV. 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Tian H, Liu L, Wu Y, Wang R, Jiang Y, Hu R, et al. Respir Res. Furusho T, Uchida S, Sohara E. The WNK signaling pathway and salt-sensitive hypertension. Hypertens Res. Sohara E, Uchida S. Nephrol Dial Transplant. Carmichael C, Wainford R. Brain G α i2-subunit proteins and the prevention of salt sensitive hypertension. Wainford RD, Carmichael CY, Pascale CL, Kuwabara JT. Gαi2-protein—mediated signal transduction. Ohtsu H, Suzuki H, Nakashima H, Dhobale S, Frank GD, Motley ED, et al. Angiotensin II signal transduction through small GTP-binding proteins. Paravicini TM, Touyz RM. Redox signaling in hypertension. Kapuku GK, Ge D, Vemulapalli S, Harshfield GA, Treiber FA, Snieder H. Change of genetic determinants of left ventricular structure in adolescence: longitudinal evidence from the Georgia cardiovascular twin study. Arnett DK, Hong Y, Bella JN, Oberman A, Kitzman DW, Hopkins PN, et al. Post WS, Larson MG, Myers RH, Galderisi M, Levy D. Heritability of left ventricular mass. Vasan RS, Glazer NL, Felix JF, Lieb W, Wild PS, Felix SB, et al. Genetic variants associated with cardiac structure and function: a meta-analysis and replication of genome-wide association data. Petretto E, Sarwar R, Grieve I, Lu H, Kumaran MK, Muckett PJ, et al. Integrated genomic approaches implicate osteoglycin ogn in the regulation of left ventricular mass. Nat Genet. Gudbjartsson DF, Arnar DO, Helgadottir A, Gretarsdottir S, Holm H, Sigurdsson A, et al. Variants conferring risk of atrial fibrillation on chromosome 4q Bapat A, Anderson CD, Ellinor PT, Lubitz SA. Genomic basis of atrial fibrillation. Sinner MF, Tucker NR, Lunetta KL, Ozaki K, Smith JG, Trompet S, et al. Integrating genetic, transcriptional, and functional analyses to identify 5 novel genes for atrial fibrillation. Iwasaki Y, Nishida K, Kato T, Nattel S. Atrial fibrillation pathophysiology. Campbell HM, Wehrens XHT. Genetics of atrial fibrillation: an update. Lieb W, Jansen H, Loley C, Pencina MJ, Nelson CP, Newton-Cheh C, et al. Genetic predisposition to higher blood pressure increases coronary artery disease risk. Lu X, Huang J, Wang L, Chen S, Yang X, Li J, et al. Genetic predisposition to higher blood pressure increases risk of incident hypertension and cardiovascular diseases in Chinese. Kaviarasan V, Mohammed V, Veerabathiran R. Genetic predisposition study of heart failure and its association with cardiomyopathy. Egypt Heart J. Pazoki R, Dehghan A, Evangelou E, Warren H, Gao H, Caulfield M, et al. Genetic predisposition to high blood pressure and lifestyle factors. Treatment for hypertensive heart disease depends on the seriousness of your illness, your age, and your medical history. Medications help your heart in a variety of ways. The main goals are to prevent your blood from clotting, improve the flow of your blood, and lower your cholesterol. In more extreme cases, you may need surgery to increase blood flow to your heart. A pacemaker produces electrical stimulation that causes cardiac muscle to contract. Implantation of a pacemaker is important and beneficial when cardiac muscle electrical activity is too slow or absent. Cardioverter-defibrillators ICDs are implantable devices that can be used to treat serious, life-threatening cardiac arrhythmias. Coronary artery bypass graft surgery CABG treats blocked coronary arteries. This is only done in severe CHD. A heart transplant or other heart-assisting devices may be necessary if your condition is especially severe. Recovering from hypertensive heart disease depends on the exact condition and its intensity. Lifestyle changes can help keep the condition from getting worse in some cases. In severe cases, medications and surgery may not be effective in controlling the disease. Monitoring and preventing your blood pressure from getting too high is one of the most important ways to prevent hypertensive heart disease. Lowering your blood pressure and cholesterol by eating a healthy diet and monitoring stress levels are possibly the best ways to prevent heart problems. Maintaining a healthy weight, getting adequate sleep, and exercising regularly are common lifestyle recommendations. Talk to your doctor about ways to improve your overall health. Hypertensive heart disease is a serious condition that requires treatment. It increases your risk of death and puts you at risk of developing other cardiovascular diseases like heart failure, atrial fibrillation, and stroke, as well as chronic kidney disease. Long-term high blood pressure ultimately leads to heart damage, and often heart failure. The length of time to develop heart damage varies for each person and depends on how uncontrolled your blood pressure is and what markers are used to determine LV damage. Treatment of high blood pressure can help prevent damage to the heart. A study found that after 6 months of treatment, a person had succeeded in reversing heart damage caused by hypertension. Following a well-development treatment plan can help you manage symptoms and prevent disease progression. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Congenital heart disease, also known as congenital heart defect, is a heart abnormality present at birth. Learn about its symptoms, causes, and…. Your heart keeps you alive and well, and protecting its health should be a top priority. Here are 18 heart-healthy snacks and drinks. What you eat is key to keeping your heart healthy. Here are the 6 best diets for heart health. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Hypertensive Heart Disease. Medically reviewed by Angela Ryan Lee, MD, FACC — By Chitra Badii — Updated on February 12, Types of hypertensive heart disease. Who is at risk for hypertensive heart disease? Identifying the symptoms of hypertensive heart disease. Testing and diagnosis: When to see the doctor. Treating hypertensive heart disease. Long-term outlook. Preventing hypertensive heart disease. Frequently asked questions. How we reviewed this article: Sources. |
| Blood pressure and heart failure | Export disfase EndNote Hypertension and heart disease Manager Hypertension and heart disease TEXT file BibTex. van Balanced snacking choices E, Hypertenison PA, de Theije Thyroid Strengthening Formulas, Babiker FA, Molkentin JD, de Windt LJ. High Blood Pressure. A Mayo Clinic expert explains. What is aortic aneurysm? High blood pressure, also called hypertension, can quietly damage the body for years before symptoms appear. |
| High blood pressure (hypertension) - Symptoms & causes - Mayo Clinic | From Mayo Clinic to your abd. Worldwide trends in hypertension prevalence and progress Hypertendion treatment and control from to a pooled analysis heqrt Balanced snacking choices studies with herbal wakefulness supplements participants. Balanced snacking choices GW, Fung JW, Tan YT, Sanderson JE. Lip S, Tan LE, Jeemon P, McCallum L, Dominiczak AF, Padmanabhan S. Healthy lifestyle habits —such as not smoking, exercising and eating well — can help prevent and treat high blood pressure. About this article. Felder RA, Gildea JJ, Xu P, Yue W, Armando I, Carey RM, et al. |
| Rates of High Blood Pressure Control Vary by Sex and Race | Guidelines can change as new information becomes available, Therefore, your health care provider may recommend more frequent screenings based on your blood pressure levels and other health conditions. Bakris GL, Sorrentino MJ. Systemic hypertension: mechanisms, diagnosis, and treatment. In: Libby P, Bonow RO, Mann DL, Tomaselli GF, Bhatt DL, Solomon SD, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, PA: Elsevier; chap Rogers JG, O'Connor CM. Heart failure: pathophysiology and diagnosis. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. Siu AL, US Preventive Services Task Force. Screening for high blood pressure in adults: US Preventive Services Task Force recommendation statement. Ann Intern Med. PMID: pubmed. Victor RG. Arterial hypertension. Whelton PK, Carey RM, Aronow WS, et al. J Am Coll Cardiol. Reviewed by: Michael A. Chen, MD, PhD, Associate Professor of Medicine, Division of Cardiology, Harborview Medical Center, University of Washington Medical School, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A. Editorial team. Share Facebook Twitter Linkedin Email Home Health Library. Hypertensive heart disease Hypertension - hypertensive heart; High blood pressure - hypertensive heart. High BP increases the left ventricular LV afterload and peripheral vascular resistance, and prolonged exposure to an increased load leads to pressure- and volume-mediated LV structural remodeling [ 2 , 10 ]. Ventricular hypertrophy is an initial compensatory mechanism in response to the chronic pressure overload that preserves the cardiac output and delays cardiac failure. However, the remodeled left ventricle is likely to decompensate, and HF can develop as a consequence of increased LV stiffness and the presence of diastolic dysfunction [ 11 ]. Diastolic dysfunction is one of the first changes observed in a heart that has been exposed to an increased load. In response to LV end-diastolic pressure elevations, the left ventricle becomes hypertrophied and more rigid, and additional changes are induced by neurohormonal pathways activated by the BP increase [ 12 ]. Ventricular hypertrophy can be divided into either concentric or eccentric hypertrophy by relative wall thickness RWT. A long-standing pressure overload is more likely to develop into concentric hypertrophy, while a volume overload is associated with eccentric hypertrophy. In chronic HTN, which involves both pressure and volume overloads, the LV hypertrophy can be concentric or eccentric, and these types are associated with HF with a preserved ejection fraction HFpEF and HF with a reduced ejection fraction HFrEF , respectively. Demographic factors affect the response of the ventricle; hence, black patients are more likely than white patients to have concentric responses [ 14 ], and female and older patients are more prone to concentric changes [ 15 , 16 ]. Patients with isolated systolic HTN and those with higher systolic BPs SBPs and ambulatory BPs are also more likely to exhibit concentric hypertrophy [ 17 , 18 ]. Comorbid conditions can also affect the patterns of hypertrophy. For example, patients with diabetes are more prone to concentric changes [ 19 ], while patients with coronary artery disease and those who are obese are more likely to exhibit eccentric remodeling [ 20 , 21 ]. Furthermore, the activation of neurohormonal pathways, including the renin-angiotensin system and the sympathetic nervous system [ 22 ], and extracellular matrix alterations induce changes in the ventricular mass and dimension [ 23 ]. Hypertensive HF primarily manifests as diastolic dysfunction, followed by concentric or eccentric LV hypertrophy. Diastolic dysfunction increases the LV filling pressure and left atrial LA volume, which, in turn, increase the pulmonary artery pressure [ 24 ]. The pathway from LV hypertrophy to overt HF is complex and unclear. Most patients with concentric hypertrophy develop HFpEF, but despite the absence of a history of myocardial infarction, some can progress to HFrEF. The development of HFpEF seems to be associated with changes in the extracellular matrix that cause progressive fibrosis of the myocardium and, subsequently, an increase in LV stiffness [ 25 ]. It is also possible that patients with eccentric LV hypertrophy will progress to either HFpEF or HFrEF. Cardiac structural changes are mostly caused by a chronic rise in the BP, and they are markers of preclinical or asymptomatic CV disease [ 27 ]. The presence of an LV strain pattern, that is, LV hypertrophy, on a lead electrocardiogram is an independent predictor of the CV outcome [ 28 ]. The findings from two-dimensional echocardiography suggest that LV hypertrophy is a significant predictor of mortality [ 29 ]. Ventricular hypertrophy is also a major predictor of stroke and renal outcomes [ 31 ]. Echocardiography can also detect diastolic dysfunction, and it provides information about chamber geometry and systolic function. Patients with long-standing HTN are more sensitive to changes in pressure, volume, and sympathetic tone [ 33 ]. Although decompensated HF is usually considered a volume-overloaded state provoked by poor systolic function, the excess volume may not always be required for a patient to present with HF in those with LV hypertrophy and diastolic dysfunction. The reduced compliance of the ventricle and systemic vasculature in patients with hypertensive HF results in abnormal ventricular-vascular interactions [ 34 ]. The premature return of aortic pulse waves increases the resistance to the ventricular outflow, which, in turn, impedes the pulmonary venous flow towards the heart [ 33 ]. Consequently, small changes in the preload, afterload, or sympathetic tone can further increase the LV filling pressure, thereby disrupting the pulmonary capillary blood-gas barrier, which leads to flash pulmonary edema [ 12 ]. Hypertensive acute HF occurs when adverse conditions result in a volume redistribution and a shift from the splanchnic and peripheral vasculature to the pulmonary circulation. This ventricular-vascular uncoupling manifests as a rapid onset of pulmonary edema in patients with LV hypertrophy and diastolic dysfunction. Although intravenous diuretics are the first choice in treating acute HF with volume overload Class I , reducing the preload and afterload using vasodilators Class IIa, LOE B should be also considered, as the volume overload might not be involved in the clinical congestion in some patients [ 33 ]. The prevalence of HTN as an HF etiology varies geographically and temporally Table 1. The findings from the Korean Heart Failure KorHF study, which recruited patients with HF from to , showed that In contrast, the presence of HTN as a comorbid condition in patients with HF has become more pronounced over time. The frequent coexistence of HTN and HF is observed across all regions. Indeed, Insurance claims data from the United States of America suggest that HTN was the most commonly co-occurring clinical condition among Medicare beneficiaries with HF [ 48 ]. Whether HTN is a cause or a contributor to the development of HF is not clear. Although a BP elevation alone may not be sufficient to trigger HF, it increases the risk of CV diseases progressing to HF. For example, the activation of neurohormonal pathways induced by a persistent BP elevation in addition to LV hypertrophy could lead to adverse modifications of postinfarct ventricular remodeling, rendering the heart vulnerable to the development of HF after a myocardial infarction [ 49 ]. Factors, including an increased afterload, reduced arterial compliance, and the lack of a response to vasodilators, also affect cardiac output in the context of HF [ 50 ]. Two issues arise regarding HF when treating HTN. The first is strictly controlling high BP to prevent structural remodeling and the development of HF. The presence of a J-curve association between BP and CV outcomes have been long debated, but evidence has been controversial [ 51 , 52 ]. The current consensus is that strict control is mostly beneficial for hypertensive patients with low CV risk, while the risk of CV outcome increases in patients with high risk for coronary heart disease [ 53 ]. BP lowering in patients with ventricular hypertrophy can delay further remodeling and reduce the incidence of HF [ 55 ]. The LV hypertrophy induced by HTN is not unidirectional, and a regression of LV mass has been observed after the pharmacological treatment of elevated BP [ 43 ]. Improvements in LV hypertrophy have also been associated with reduced risks of CV events, including CV death, myocardial infarction, and stroke [ 56 ]. Identifying patients at an increased risk of developing hypertensive HF is important to enable attentive monitoring and begin timely treatment. LA enlargement in the absence of mitral valve disease could be a marker of diastolic dysfunction; this has been demonstrated by the correlation between the LA volume and the natriuretic peptide levels in asymptomatic patients with preserved systolic function [ 57 ]. Biomarkers such as uric acid, metalloproteinases, and natriuretic peptides, may also predict the development of HF in patients with HTN [ 58 ]. Patients with HTN and a high clinical risk of HF should be screened regularly for diastolic dysfunction or LV hypertrophy to prevent progression to advanced disease. A meta-analysis of randomized clinical trials that analyzed HF as an outcome showed significant reductions in the new-onset HF rates in association with all of these classes of drug, except for ARBs, which may have been a consequence of the small number trials reviewed. Thiazide-like diuretics, which are widely used to treat HTN, but are not frequently used in patients with HF, also reduced the new-onset HF rate compared with placebo [ 60 ], which suggests that reducing the BP itself is probably the most important factor in HF prevention. Currently, no specific class of drugs is recommended for the prevention of HF in patients with HTN, and patients should be treated according to the guidelines [ 61 ]. The other issue regarding HF and HTN is managing high BP in established HF patients. As all medications that have favorable effects on HF outcomes lower BP to some extent, we can assume that a close relationship exists between BP and HF outcomes. However, data describing the optimal BP in patients with HF are limited and contradictory. The findings from the OPTIMIZE-HF Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure trial suggested that BP elevations in patients with HF were associated with lower in-hospital mortality rates [ 46 , 62 ]. A meta-analysis of patients with chronic HF also confirmed a trend towards better outcomes in patients with higher BPs [ 63 ]. However, the findings of a recent prospective cohort study has demonstrated that a higher SBP, diastolic BP, and pulse pressure were associated with higher rates of adverse events among patients with incident HF [ 67 ]. The relationship between BP and the HF prognosis is not necessarily always linear. A J-curve that is similar to that which describes the relationship between the BP and CV outcomes, has been indicated repeatedly in patients with HTN [ 68 , 69 , 70 ]. The findings from a study of the KorAHF registry showed that a reverse J-curve relationship was evident between the treatment of BP and the outcomes of patients who were hospitalized for HF [ 71 ], and that the risks of mortality and readmission increased at low and high BPs, with similar trends for patients with HFrEFs and HFpEFs Fig. Restricted Cubic Splines Model for All-Cause Mortality According to On-Treatment BP. a SBP: all population. b SBP: heart failure with reduced ejection fraction EF. c SBP: heart failure with preserved EF. d DBP: all population. e DBP: heart failure with reduced EF EF. f DBP: heart failure with preserved EF. SBP, systolic blood pressure; DBP, diastolic blood pressure. Reprinted from JACC: Heart Failure, Vol 5, Lee SE, et al. The trade-off between prescribing adequate doses of guideline-directed medical treatments and maintaining a lower BP threshold is an issue that many physicians encounter in daily practice. The benefits of treatment in relation to the outcomes must be weighed against the adverse effects induced by lower BPs. Although medications with survival benefits remain effective within lower BP thresholds, no definitive evidence is available that supports intensive BP treatment. The current evidence suggests that all patients with HF should receive triple therapy comprising ACE inhibitors or ARBs, beta-blockers, and diuretics, with the doses adjusted to maintain an adequate BP, and if a patient remains hypertensive, thiazide-like diuretics can be added [ 12 ]. Among patients with chronic HTN, structural and functional changes in the heart can lead to the development of HF. BP management not only prevents asymptomatic HTN-mediated organ damage that can cause HF but can also prevent further disease progression. The intensive control of BP is recommended for patients with HTN who are at risk of HF; however, the optimal range within which BP should be controlled and the benefits of intensive BP control in patients with established HF remain unclear. World Health Organization Global Health Observatory GHO data. Accessed 18 Sept Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. Article PubMed CAS Google Scholar. Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol. McLenachan JM, Henderson E, Morris KI, Dargie HJ. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med. Vasan RS, Larson MG, Leip EP, Evans JC, O'Donnell CJ, Kannel WB, et al. 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Hypertension and heart disease -
Further, lifestyle modifications have also been reported to be beneficial To alleviate heart failure and reduce its complications, several interventions are available For example, in a clinical trial by Hieda et al.
they found that physical exercise training for one year reversed left ventricular myocardial stiffness in patients with stage B heart failure with preserved ejection fraction that is characterized by LVH and N-terminal pro-B-type natriuretic peptide or high-sensitivity troponin Therapeutic interventions for patients with heart failure also exist.
Empagliflozin, dapagliflozin and spironolactone improves and ameliorates adverse outcomes of heart failure with persevered ejection fraction — In addition, individualized nutritional support as well as treatment with vericiguat for hospitalized patients with heart failure is also beneficial in reducing the risk for death and morbidity — Further, in patients with acute decompensated heart failure, usage of levosimendan in combination with Shenfu injection was effective in improving hemodynamics and enhance myocardial contractility In severe heart failure where therapy is limited, use of omecamtiv mecarbil therapy is reported to have beneficial effects in reducing adverse outcomes Management of heart failure is discussed in detail in the US and European guidelines.
Future studies should focus on clinical studies especially prospective to understand the pathogenesis and complications of hypertensive heart disease as there are few studies in this area. Understanding the implications of physiological and pathological LVH and the potential for regression will be important for clinical application.
Hypertensive heart disease progresses through several mechanisms that amplify and increase the risk for adverse complications. Excess dietary salt is one of the modifiable factors that contribute enormously to the pathogenesis of hypertensive heart disease.
Reduction of dietary salt has potential to reduce blood pressure and the risk for development of hypertensive heart disease. SM: conceptualized the study and wrote the draft manuscript. SM and AK: wrote and edited different sections of the manuscript. SM: created all the figures.
AK: conceptualized the frame-work and finalized the manuscript as well as obtained funding for the manuscript.
All authors contributed to the article and approved the submitted version. This work was supported by the Fogarty International Center of the National Institutes of Health grants R03HL, R01HL and R01HL AK and 2D43TW SM.
The content is solely the responsibility of the authors and does not represent the official views of the National Institutes of Health. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
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That's because limited blood flow caused by high blood pressure can block blood from flowing to the penis. High blood pressure can reduce blood flow to the vagina. Reduced blood flow to the vagina can lead to less sexual desire or arousal, vaginal dryness, or trouble having orgasms.
High blood pressure usually is an ongoing condition that slowly causes damage over years. But sometimes blood pressure rises so quickly and seriously that it becomes a medical emergency. When this happens, treatment is needed right away, often with hospital care.
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Request Appointment. High blood pressure dangers: Hypertension's effects on your body. Products and services. High blood pressure dangers: Hypertension's effects on your body High blood pressure is a risk factor for more than heart disease. By Mayo Clinic Staff.
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