About this Journal Submit a Manuscript Table of Contents
ISRN Hypertension
Volume 2013 (2013), Article ID 410740, 8 pages
http://dx.doi.org/10.5402/2013/410740
Review Article

Hypertensive Patients and Their Management in Dentistry

1Department of Oral Rehabilitation and Dental Prosthodontics, Faculty of Dental Medicine, University of Medicine and Pharmacy, Petru Rares No. 2–4, 200349 Craiova, Romania
2Department of Odontotherapy, Endodontics and Orthodontics, Faculty of Dental Medicine, University of Medicine and Pharmacy, 1 Mai No. 68, Craiova, Romania

Received 1 October 2013; Accepted 22 October 2013

Academic Editors: F. Angeli and K. C. Ortega

Copyright © 2013 Sanda Mihaela Popescu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Hypertension is a common disease encountered in dental setting. Its wide spreading, terrible consequences, and life-long treatment require an attentive approach by dentists. Hypertension management in dental office includes disease recognition and correct measurement, knowledge of its treatment and oral adverse effects, and risk assessment for dental treatment. Dentist role in screening undiagnosed and undertreated hypertension is very important since this may lead to improved monitoring and treatment.

1. Introduction

Hypertension is defined as values >140 mmHg SBP and/or >90 mmHg DBP, based on the evidence from RCTs that in patients with these BP values treatment-induced BP reductions are beneficial (Table 1) [1]. The same classification is used in young, middle-aged, and elderly subjects, whereas different criteria, based on percentiles, are adopted in children and teenagers for whom data from interventional trials are not available [1].

tab1
Table 1: Definitions and classification of office blood pressure levels (mmHg)a [1].

JNC 7 introduced in 2003 the category of prehypertension, which is defined as SBP of 120 to 139 mmHg and DBP of 80 to 89 mmHg (Table 2) [2]. Patients with prehypertension are at increased risk of developing hypertension, those with blood pressure values 130–139/80–89 mmHg have a two times greater risk of developing hypertension than those with lower values [3].

tab2
Table 2: JNC 7 classification of hypertension [2].

Hypertension is a highly prevalent cardiovascular disease, which affects over 1 billion people worldwide [2]. Although more than 70% of hypertensive patients are aware of the disease, only 23–49% are treated, and fewer (20%) achieving control [2, 4, 5]. Hypertension prevalence varies by age, race, education, and so forth.

According to ESC-ESH guidelines in 2013, there are limited comparable data available on the prevalence of hypertension and the temporal trends of BP values in different European countries [6]. Overall the prevalence of hypertension appears to be around 30–45% of the general population, with a steep increase with ageing. There also appear to be noticeable differences in the average BP levels across countries, with no systematic trends towards BP changes in the past decade [729].

A permanent high blood pressure (BP) affects blood vessels in the kidneys, heart, and brain, increasing the incidence of renal and cardiac coronary heart disease and stroke. Hypertension was called the “silent killer” because it often affects target organs (kidney, heart, brain, eyes) before the appearance of clinical symptoms.

2. Etiology and Classification of Hypertension

Hypertension is classified as primary or essential hypertension (without an organic cause) and secondary hypertension (it has a well-established organic cause).

2.1. Primary or Essential Hypertension (without an Organic Cause)

Primary hypertension is the term used for medium to high BP for a long time (chronic) without a known cause, which is a very common form of hypertension, comprising about 90–95% of all patients with hypertension [30].

2.2. Secondary Hypertension

Hypertension with an organic cause, well established the following:(i)renal (parenchyma or renal vascular) chronic pyelonephritis, acute and chronic glomerulonephritis, polycystic kidney disease, renal vascular stenosis or renal infarction, other severe kidney disease (arteriolar nephrosclerosis), renin-secreting tumors;(ii)endocrine: oral contraceptives, adrenal hyper function (Cushing’s syndrome, primary aldosteronism, congenital or hereditary adrenogenital syndrome), pheochromocytoma, myxedema, acromegaly, thyroid and parathyroid hyper function;(iii)neurological: psychogenic “diencephalic syndrome,” familiar dysautonomia (Riley-Day), polyneuritis (acute porphyria, lead poisoning), increased intracranial pressure;(iv)others: coarctation of the aorta, increased intravascular volume (transfusion excessive polycythemia vera), polyarteritis, hypercalcemia, drugs (corticosteroids, cyclosporine), sleep apnea, pregnancy toxemia, acute intermittent porphyria.

3. Pathogenesis of Essential Hypertension

From family and epidemiological studies it is clear that hypertension results from a complex interaction between genetic factors and the environment [31]. There are at least 50 known factors which increase blood pressure, among which the most important are [32, 33]:(i)age (over 55 years for men, over 65 years for women);(ii)a family history of premature cardiovascular disease;(iii)smoking;(iv)increased consumption of alcohol;(v)sedentariness;(vi)cholesterol rich diet;(vii)coexistence of other diseases (diabetes, obesity, dyslipidemia).

4. Treatment of Hypertension

Adopting a healthy lifestyle is critical in preventing high blood pressure. The major changes in lifestyle that could lead to lower blood pressure include reduction of body weight in overweight or obese patients [34], adopting a low-salt diet [35] rich in potassium and calcium [36], increasing physical activity [37], moderate alcohol consumption [37], and smoking cessation [38].

Hypertension drug treatment depends on the stage of hypertension, associated diseases, and risk factors present. Recommendations are based on the definition and classification of hypertension adopted by The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure in USA in 2003 [2] and the conclusions of the European Society of Hypertension-European Society of Cardiology (ESH-ESC) in 2013 [1]. They determine the maximum physiological BP 130 mmHg systolic and 85 mmHg for diastolic, BP values of 139 mmHg systolic, and 89 mmHg diastolic standing at the upper limit of normal. The recommendations emphasize that the decision to drop blood pressure in a particular patient should not rely solely on the values of BP but also on total cardiovascular risk assessment of that patient (Table 3). From the meta-analysis by Staessen et al. [39] results show that all classes of antihypertensive agents provide similar cardiovascular protection. To prevent stroke and congestive heart failure, feared complications of hypertension, the results of recently published trials suggest that some classes can achieve selective benefits.

tab3
Table 3: Total cardiovascular risk assessment [1].
4.1. Total Cardiovascular Risk Assessment [1]

ESC-ESH report from June 2013 presents SCORE model of assessment of total cardiovascular risk using charts and interactive site http://www.heartscore.org. The charts must be interpreted considering physician’s knowledge and experience [1]. Risk may be higher than indicated in the charts in the following:(1)sedentary subjects and those with central obesity; the increased relative risk associated with overweight is greater in younger subjects than in older subjects;(2)socially deprived individuals and those from ethnic minorities;(3)subjects with elevated fasting glucose and/or an abnormal glucose tolerance test, who do not meet the diagnostic criteria for diabetes;(4)individuals with increased triglycerides, fibrinogen, apolipoprotein B, lipoprotein levels, and high-sensitivity C-reactive protein;(5)individuals with a family history of premature CVD (before the age of 55 years in men and 65 years in women).

Three important causes of primary hypertension are salt/volume overload, activation of the reninangiotensin-aldosterone system (RAAS), and activation of the sympathetic nervous system (Table 4) [4].

tab4
Table 4: Mechanisms implicated in essential hypertension and antihypertensive medication classes targeting these mechanisms [4].

Salt (sodium chloride) overload/volume overload is one of the common causes of hypertension. Essential hypertension has been associated with high sodium intake in a variety of scientific models, clinical studies and trials, and it is certified that decreasing the sodium intake ameliorates this effect [40, 41]. High sodium intake increases blood pressure by expanding intravascular volume and may have direct neurohormonal effects on the cardiovascular system [4, 41]. Thiazide diuretics are indicated by JNC 7 [2] as initial therapy for most patients with hypertension, either alone or in combination with another class of antihypertensive agents.

The “Renin Angiotensin Aldosterone System” (RAAS) hormonal axis also contributes to hypertension in many patients [4]. Renin, a hormone synthesized and released by the kidney in response to intravascular volume depletion and hyperkalemia, promotes the conversion of angiotensinogen (produced by the liver) to angiotensin I, which is converted to angiotensin II by the angiotensin-converting enzyme (ACE) in the lung. One mechanism of increasing blood pressure by angiotensin II is increasing renal sodium reabsorption, producing vasoconstriction, and activating the sympathetic nervous system [4]. But angiotensin II also increases the production and secretion of aldosterone from the adrenal cortex, and aldosterone increases renal sodium reabsorption [4]. Thus, the RAAS system increases blood pressure through increasing renal sodium reabsorption (which leads to intravascular volume expansion) and vasoconstriction.

There are several classes of medications used to block various components of the RAAS pathway, like β-Blockers such as propranolol, carvedilol, and metoprolol (decrease renal renin release), direct renin inhibitor aliskiren (binds to renin and thus prevents the conversion of angiotensinogen to angiotensin I), ACE inhibitors (block ACE and prevent the conversion of angiotensin I to angiotensin II), angiotensin II receptor blockers (prevent angiotensin II from binding to its receptor, decreasing vasoconstriction and renal sodium reabsorption), aldosterone-receptor blockers (such as spironolactone and eplerenone), and other medications such as amiloride (decrease the effects of aldosterone-mediated renal sodium reabsorption) [4].

Activation of the sympathetic nervous system (SNS) also contributes to the development, maintenance, and progression of hypertension. Therapies have been developed to target the central, peripheral, and renal SNS to improve the control of blood pressure: peripheral α1-receptor blockers (such as terazosin and tamsulosin), central α2-agonist clonidine, and β-blockers, vasodilators such as minoxidil, nitrates, and hydralazine [2, 42].

5. Oral Manifestations Caused by the Adverse Effects of Antihypertensive Drugs

5.1. Xerostomia

Many antihypertensives medications like ACEIs, thiazide diuretics, loop diuretics, and clonidine are associated with xerostomia [4346]. Its likelihood increases with the number of concomitant medications. Xerostomia has many consequences, like decay, difficulty in chewing, swallowing, and speaking, candidiasis, and oral burning syndrome. Sometimes the feeling is transient and salivary function is adjusted by the patient itself. There are situations when is required to change the antihypertensive medication. It is often necessary to treat xerostomia directly with parasympathomimetic agents such as pilocarpine or cevimeline. Other recommendations include frequent sipping of water, sugarless candies, coffee consumption reduction, and avoiding alcohol containing mouthwashes. To reduce the risk of caries topical applications of fluoride, particularly in the form of gels with high concentrations applied by brush or trays [47], are recommended.

5.2. Gingival Hyperplasia

It can be caused by calcium channel blockers, with an incidence ranging from 6 to 83% [4852]. The majority of cases are associated with nifedipine. The effect could be dose related. Gingival hyperplasia is manifested by pain, gingival bleeding, and difficulty in mastication. A good oral hygiene greatly reduces its incidence. By changing antihypertensive medication hyperplasia can be reversed [53].

5.3. Lichenoid Reaction

Many antihypertensives (thiazide diuretics, methyldopa, propranolol, captopril, furosemide, spironolactone, and labetalol) are associated with oral lichenoid reactions [54, 55]. Clinical forms differ greatly from lichen planus itself. The easiest way to treat it is to change antihypertensive medication, and lichenoid reactions are resolving after discontinuation of the responsible drug. If medication could not be changed, lichenoid reactions are treated with topical corticosteroids [47].

5.4. Other Undesirable Effects

ACE inhibitors are associated with cough and loss of taste (ageusia) or taste alteration (dysgeusia). Dysgeusia has also been reported with other antihypertensives use, like β-blockers, acetazolamide, and diltiazem. It has been postulated that dysgeusia may result through a mechanism affecting salivary handling of metal ions such as magnesium [56, 57].

6. Drug Interactions between Antihypertensives and Drugs Used in Dentistry

Most antihypertensive drugs have drug interactions with LA (local anesthetic) and analgesics.(i)Interaction of LA with nonselective beta-blockers may increase LA toxicity [58].(ii)The cardiovascular effects of epinephrine used during dental procedures may be potentiated by the use of medications such as nonselective b-blockers (propranolol and nadolol). Guidelines recommend decreasing the dose and increasing the time interval between epinephrine injections [59].(iii)Long-term use of NSAIDs may antagonize the antihypertensive effect of diuretics, beta-blockers, alpha blockers, vasodilators, ACE inhibitors [4]. Short-term administration has, however, a clinically meaningful effect. Other pain relievers such as paracetamol can be used to avoid this side effect.

Dental treatment in hypertensive patients necessitates special attention, because any stressful procedure may increase blood pressure and trigger acute complications such as cardiac arrest or stroke.

Control of pain and anxiety is very important in patients with high medical risk. Patients with cardiovascular disease have a high risk of complications due to endogenous catecholamines (adrenaline and noradrenaline) released from pain and stress. These catecholamines may increase dramatically BP and cardiac output. This effect is reduced by controlling dental pain. Local anesthetics with epinephrine produce a longer and more effective anesthesia than simple LA, thus avoiding an exaggerated response to stress [60]. LA with vasoconstrictor should be avoided or used in low doses in patients taking nonselective beta-blockers or in patients with uncontrolled hypertension. The maximum recommended dose of epinephrine in a patient with cardiac risk is 0.04 mg, which is equal to that containing about two cartridges of LA with 1 : 100000 epinephrine or 4 cartridges with 1 : 200000 epinephrine [60]. In patients with severe disease it may be useful to measure BP and heart rate after anesthetic injection. Slow administration and aspiration can prevent undesirable reactions.

Other contraindications to vasoconstrictor AL include severe uncontrolled hypertension, refractory arrhythmias, myocardial infarction or stroke by age less than 6 months, unstable angina, coronary artery bypass graft under 3 months, congestive heart failure, and untreated hyperthyroidism [61].

Due to higher concentrations of epinephrine (almost 12 standard cartridges) in gingival retraction cords used for prosthetics impressions and its rapid uptake in circulation, the use of epinephrine for gingival eviction in patients with cardiovascular disease is contraindicated [4, 62].

7. Hypertensive Patient Management in the Dental Office

Initial evaluation of each patient with hypertension should include detailed family history of cardiovascular disease and other related diseases, history of hypertension, medications, duration and antihypertensive treatment history, severity of disease, and its complications [61]. Before starting dental treatment, dentist has to assess the presence of hypertension, to determine the presence of associated organ disease and determine dental treatment changes needed [63].

Particular attention should be given to accurate measurement of BP in pregnant women, since pregnancy may alter the patient BP values, more than 10% of pregnant women having clinically relevant hypertension [64]. BP monitoring is also necessary in diabetic patients, patients with autonomous dysfunction, and elderly patients for which orthostatic hypotension is a big problem [2]. The dentist must be familiar with other diseases treated with antihypertensive drugs (such as atenolol, amlodipine, and carteolol) as headaches, regional pain, renal failure, glaucoma, and congestive heart failure.

8. BP Measurement in the Dental Office

Patients with hypertension are at increased risk of developing adverse effects in a dental office. Therefore, measuring BP will be done in the dental office to every new patient, for each visit. In patients with chronic systemic diseases, BP measurement will be carried out during more complicated dental interventions as oral surgery, restorative treatment complicated with longer sessions, placing dental implants, and periodontal surgery.

Routine measurement of BP may reduce the risk of cardiovascular events and acute complications during dental treatment, especially when conscious sedation or general anesthesia is required. BP monitoring is vital for emergency treatment of patients who have side effects. Routine monitoring of patients with known hypertension allows the dentist to determine if BP is adequately controlled.

Best BP measurements were obtained with mercury sphygmomanometers, no longer available now. Aneroid sphygmomanometers used should be checked every 6 months. Electronics BP units are simple to use but not as accurate as the aneroid.

ESC-ESH guidelines in 2013 and JNC 7 in 2003 described the method that health care professionals should use to obtain office blood pressure measurements (Table 5) [1, 2].

tab5
Table 5: Office blood pressure measurement [1].

One must use a properly calibrated and validated blood pressure instrument. Patients should be seated in a chair with their feet on the floor for 5 minutes in a quiet room. Their arm should be supported at the level of the heart and an appropriately sized blood pressure cuff (cuff bladder encircling at least 80% of the arm) must be used. Accurate measurement of blood pressure is important to avoid overdiagnosis and underdiagnosis, as well as overtreatment and undertreatment, of hypertension [4].

9. White-Coat Hypertension, the White-Coat Effect, and Masked Hypertension

Office BP is usually higher than BP measured out of the office, which has been ascribed to the alerting response, anxiety, and/or a conditional response to the unusual situation [1]. White-coat hypertension (WCH) refers to a persistently elevated office blood pressure in the presence of a normal blood pressure outside of the office [4]. WCH is different from the white-coat effect (WCE), which refers to a high office blood pressure but whereby hypertension may or may not be present outside the office setting. Masked hypertension refers to when a patient has a normal office blood pressure but has hypertension outside of the office (Table 6). WCH, the WCE, and masked hypertension can be diagnosed through various methods including home blood pressure monitoring and 24-hour ambulatory blood pressure monitoring. WCH and masked hypertension are important for clinicians to recognize. It is controversial as to whether WCH is associated with increased cardiovascular risk, but patients with masked hypertension are at increased cardiovascular risk. The prevalence of WHC during physician visits is approximately 20% [4, 65]. The prevalence of WCH in the setting of visits to the dentist’s office has not been established. ESC-ESH guidelines recommend that the terms “white-coat hypertension” and “masked hypertension” be reserved to define untreated individuals [1].

tab6
Table 6: White-coat hypertension, the white-coat effect, and masked hypertension [4].

Routine measurement of blood pressure values in the dental office [63] is as follows:(i)measuring and recording the TA at the first visit,(ii)measuring and recording BP at recheck:(a)every two years for patients with BP < 120/80 mmHg;(b)every year for patients with BP 120–139/80–89 mmHg;(c)every visit for patients with BP > 140/90 mmHg;(d)every visit for patients with coronary artery disease, diabetes mellitus, or kidney disease with BP > 135/85 mmHg;(e)every visit for patients with established hypertension.

10. Summary

Hypertension is the most commonly diagnosed disease worldwide and is associated with increased cardiovascular risk and mortality. Many patients with hypertension have uncontrolled disease. The dentist has an important role in screening undiagnosed and undertreated hypertension, which may lead to improved monitoring and treatment. It is generally recommended that emergency dental procedures be avoided in patients with a blood pressure of greater than 180/110 mmHg. Because of the high prevalence of disease and medication use for hypertension, dentists should be aware of the oral side effects of antihypertensive medications. Also, dentists should consider management of drug-drug interactions of antihypertensives with medications commonly used during dental visits.

References

  1. G. Mancia, R. Fagard, K. Narkiewicz et al., “ESH/ESC guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European society of hypertension (ESH) and of the European society of cardiology (ESC),” Journal of Hypertension, vol. 25, no. 9, pp. 1751–1762, 2007. View at Publisher · View at Google Scholar · View at Scopus
  2. A. V. Chobanian, G. L. Bakris, H. R. Black et al., “The seventh report of the joint national committee on prevention, detection, evaluation and treatment of high blood pressure: the JNC 7 report,” Journal of the American Medical Association, vol. 289, no. 19, pp. 2560–2572, 2003. View at Publisher · View at Google Scholar · View at Scopus
  3. R. S. Vasan, M. G. Larson, E. P. Leip et al., “Impact of high-normal blood pressure on the risk of cardiovascular disease,” The New England Journal of Medicine, vol. 345, no. 18, pp. 1291–1297, 2001. View at Publisher · View at Google Scholar · View at Scopus
  4. J. Hogan and J. Radhakrishnan, “The assessment and importance of hypertension in the dental setting,” Dental Clinics of North America, vol. 56, pp. 731–745, 2012. View at Google Scholar
  5. M. Dorobantu, R. O. Darabont, E. Badila, and S. Ghiorghe, “Prevalence, awareness, treatment, and control of hypertension in Romania: results of the SEPHAR study,” International Journal of Hypertension, vol. 2010, Article ID 970694, 6 pages, 2010. View at Publisher · View at Google Scholar
  6. M. Pereira, N. Lunet, A. Azevedo, and H. Barros, “Differences in prevalence, awareness, treatment and control of hypertension between developing and developed countries,” Journal of Hypertension, vol. 27, no. 5, pp. 963–975, 2009. View at Publisher · View at Google Scholar · View at Scopus
  7. N. Danon-Hersch, P. Marques-Vidal, P. Bovet et al., “Prevalence, awareness, treatment and control of high blood pressure in a Swiss city general population: the co laus study,” European Journal of Cardiovascular Prevention and Rehabilitation, vol. 16, no. 1, pp. 66–72, 2009. View at Publisher · View at Google Scholar · View at Scopus
  8. B. Altun, M. Arici, G. Nergizoglu et al., “Prevalence, awareness, treatment and control of hypertension in Turkey (the Patent study) in 2003,” Journal of Hypertension, vol. 23, no. 10, pp. 1817–1823, 2005. View at Google Scholar · View at Scopus
  9. N. T. Aytekin, K. Pala, E. Irgil, N. Akis, and H. Aytekin, “Distribution of blood pressures in Gemlik district, north-west Turkey,” Health and Social Care in the Community, vol. 10, no. 5, pp. 394–401, 2002. View at Publisher · View at Google Scholar · View at Scopus
  10. A. D. Efstratopoulos, S. M. Voyaki, A. A. Baltas et al., “Prevalence, awareness, treatment and control of hypertension in Hellas, Greece: the hypertension study in general practice in Hellas (HYPERTENSHELL) national study,” American Journal of Hypertension, vol. 19, no. 1, pp. 53–60, 2006. View at Publisher · View at Google Scholar · View at Scopus
  11. M. E. Macedo, M. J. Lima, A. O. Silva, P. Alcantara, V. Ramalhinho, and J. Carmona, “Prevalence, awareness, treatment and control of hypertension in Portugal: the PAP study,” Journal of Hypertension, vol. 23, no. 9, pp. 1661–1666, 2005. View at Google Scholar · View at Scopus
  12. T. Psaltopoulou, P. Orfanos, A. Naska, D. Lenas, D. Trichopoulos, and A. Trichopoulou, “Prevalence, awareness, treatment and control of hypertension in a general population sample of adults in the Greek EPIC study,” International Journal of Epidemiology, vol. 33, no. 6, pp. 1345–1352, 2004. View at Publisher · View at Google Scholar · View at Scopus
  13. P. A. Sarafidis, A. Lasaridis, S. Gousopoulos et al., “Prevalence, awareness, treatment and control of hypertension in employees of factories of northern Greece: the Naoussa study,” Journal of Human Hypertension, vol. 18, no. 9, pp. 623–629, 2004. View at Publisher · View at Google Scholar · View at Scopus
  14. D. B. Panagiotakos, C. H. Pitsavos, C. Chrysohoou et al., “Status and management of hypertension in Greece: role of the adoption of a mediterranean diet: the Attica study,” Journal of Hypertension, vol. 21, no. 8, pp. 1483–1489, 2003. View at Publisher · View at Google Scholar · View at Scopus
  15. J. R. Banegas, A. Graciani, J. J. de la Cruz-Troca, L. M. Leon-Munoz, P. Guallar-Castillon, and A. Coca, “Achievement of cardiometabolic targets in aware hypertensive patients in Spain: a nationwide population-based study,” Hypertension, vol. 60, pp. 898–905, 2012. View at Google Scholar
  16. P. Primatesta and N. R. Poulter, “Improvement in hypertension management in England: results from the health survey for England 2003,” Journal of Hypertension, vol. 24, no. 6, pp. 1187–1192, 2006. View at Publisher · View at Google Scholar · View at Scopus
  17. C. Meisinger, M. Heier, H. Volzke et al., “Regional disparities of hypertension prevalence and management within Germany,” Journal of Hypertension, vol. 24, no. 2, pp. 293–299, 2006. View at Publisher · View at Google Scholar · View at Scopus
  18. C. Agyemang, J. Ujcic-Voortman, D. Uitenbroek, M. Foets, and M. Droomers, “Prevalence and management of hypertension among Turkish, Moroccan and native Dutch ethnic groups in Amsterdam, the Netherlands: the Amsterdam health monitor survey,” Journal of Hypertension, vol. 24, no. 11, pp. 2169–2176, 2006. View at Publisher · View at Google Scholar · View at Scopus
  19. C. Agyemang, N. Bindraban, G. Mairuhu, G. Montfrans, R. Koopmans, and K. Stronks, “Prevalence, awareness, treatment, and control of hypertension among black surinamese, south Asian surinamese and white Dutch in Amsterdam, the Netherlands: the SUNSET study,” Journal of Hypertension, vol. 23, no. 11, pp. 1971–1977, 2005. View at Google Scholar · View at Scopus
  20. T. Scheltens, M. L. Bots, M. E. Numans, D. E. Grobbee, and A. W. Hoes, “Awareness, treatment and control of hypertension: the “rule of halves” in an era of risk-based treatment of hypertension,” Journal of Human Hypertension, vol. 21, no. 2, pp. 99–106, 2007. View at Publisher · View at Google Scholar · View at Scopus
  21. T. Zdrojewski, P. Szpakowski, P. Bandosz et al., “Arterial hypertension in Poland in 2002,” Journal of Human Hypertension, vol. 18, no. 8, pp. 557–562, 2004. View at Publisher · View at Google Scholar · View at Scopus
  22. R. Cifkova, Z. Skodova, V. Lanska et al., “Prevalence, awareness, treatment, and control of hypertension in the Czech Republic. results of two nationwide cross-sectional surveys in 1997/1998 and 2000/2001, Czech post-MONICA study,” Journal of Human Hypertension, vol. 18, no. 8, pp. 571–579, 2004. View at Publisher · View at Google Scholar · View at Scopus
  23. A. Scuteri, S. S. Najjar, M. Orru et al., “Age and gender-specific awareness, treatment, and control of cardiovascular risk factors and subclinical vascular lesions in a founder population: the Sardi NIA Study,” Nutrition, Metabolism and Cardiovascular Diseases, vol. 19, no. 8, pp. 532–541, 2009. View at Publisher · View at Google Scholar · View at Scopus
  24. M. Kastarinen, R. Antikainen, M. Peltonen et al., “Prevalence, awareness and treatment of hypertension in Finland during 1982–2007,” Journal of Hypertension, vol. 27, no. 8, pp. 1552–1559, 2009. View at Publisher · View at Google Scholar · View at Scopus
  25. E. Falaschetti, M. Chaudhury, J. Mindell, and N. Poulter, “Continued improvement in hypertension management in England: results from the health survey for England 2006,” Hypertension, vol. 53, no. 3, pp. 480–486, 2009. View at Publisher · View at Google Scholar · View at Scopus
  26. C. Erem, A. Hacihasanoglu, M. Kocak, O. Deger, and M. Topbas, “Prevalence of prehypertension and hypertension and associated risk factors among Turkish adults: Trabzon hypertension study,” Journal of Public Health, vol. 31, no. 1, pp. 47–58, 2009. View at Publisher · View at Google Scholar · View at Scopus
  27. S. Costanzo, A. Di Castelnuovo, F. Zito et al., “Prevalence, awareness, treatment and control of hypertension in healthy unrelated male-female pairs of European regions: the dietary habit profile in European communities with different risk of myocardial infarction: the impact of migration as a model of gene-environment interaction project,” Journal of Hypertension, vol. 26, no. 12, pp. 2303–2311, 2008. View at Publisher · View at Google Scholar · View at Scopus
  28. E. Cinteza and M. Balgradean, “Hypertension in Romanian children and adolescents: a cross-sectional survey,” Maedica, vol. 8, no. 1, pp. 5–10, 2013. View at Google Scholar
  29. M. Dorobanţu, R. Darabont, S. Ghiorghe et al., “Profile of the Romanian hypertensive patient data from SEPHAR II study,” Romanian Journal of Internal Medicine, vol. 50, no. 4, pp. 285–296, 2012. View at Google Scholar
  30. N. M. Kaplan, “Primary hypertension. from pathophysiology to prevention,” Archives of Internal Medicine, vol. 156, no. 17, pp. 1919–1920, 1996. View at Google Scholar · View at Scopus
  31. H. Snieder, G. A. Harshfield, and F. A. Treiber, “Heritability of blood pressure and hemodynamics in African- and European-American youth,” Hypertension, vol. 41, no. 6, pp. 1196–1201, 2003. View at Publisher · View at Google Scholar · View at Scopus
  32. M. S. Kaplan and A. Nunes, “The psychosocial determinants of hypertension,” Nutrition, Metabolism and Cardiovascular Diseases, vol. 13, no. 1, pp. 52–59, 2003. View at Google Scholar
  33. N. M. Kaplan, “Management of hypertensive patients with multiple cardiovascular risk factors,” American Journal of Hypertension, vol. 14, no. 6, part 2, pp. 221S–224S, 2001. View at Google Scholar
  34. J. He, P. K. Whelton, L. J. Appel, J. Charleston, and M. J. Klag, “Long-term effects of weight loss and dietary sodium reduction on incidence of hypertension,” Hypertension, vol. 35, no. 2, pp. 544–549, 2000. View at Google Scholar · View at Scopus
  35. W. M. Vollmer, F. M. Sacks, J. Ard et al., “Effects of diet and sodium intake on blood pressure: subgroup analysis of the DASH-sodium trial,” Annals of Internal Medicine, vol. 135, no. 12, pp. 1019–1028, 2001. View at Google Scholar · View at Scopus
  36. F. M. Sacks, L. P. Svetkey, W. M. Vollmer et al., “Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet,” The New England Journal of Medicine, vol. 344, no. 1, pp. 3–10, 2001. View at Publisher · View at Google Scholar · View at Scopus
  37. S. P. Whelton, A. Chin, X. Xin, and J. He, “Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials,” Annals of Internal Medicine, vol. 136, no. 7, pp. 493–503, 2002. View at Google Scholar · View at Scopus
  38. X. Xin, J. He, M. G. Frontini, L. G. Ogden, O. I. Motsamai, and P. K. Whelton, “Effects of alcohol reduction on blood pressure: a meta-analysis of randomized controlled trials,” Hypertension, vol. 38, no. 5, pp. 1112–1117, 2001. View at Google Scholar · View at Scopus
  39. J. A. Staessen, J. G. Wang, and L. Thijs, “Cardiovascular prevention and blood pressure reduction: a quantitative overview updated until 1 March 2003,” Journal of Hypertension, vol. 21, no. 6, pp. 1055–1076, 2003. View at Publisher · View at Google Scholar · View at Scopus
  40. A. V. Chobanian and M. Hill, “National heart, lung, and blood institute workshop on sodium and blood pressure: a critical review of current scientific evidence,” Hypertension, vol. 35, no. 4, pp. 858–863, 2000. View at Google Scholar · View at Scopus
  41. J. P. Kooman, F. M. Van der Sande, and K. M. Leunissen, “Sodium, blood pressure and cardiovascular pathology: is it all volaemia?” Nephrology Dialysis Transplantation, vol. 19, no. 5, pp. 1046–1049, 2004. View at Publisher · View at Google Scholar · View at Scopus
  42. S. J. Mann, “Drug therapy for resistant hypertension: simplifying the approach,” Journal of Clinical Hypertension, vol. 13, no. 2, pp. 120–130, 2011. View at Publisher · View at Google Scholar · View at Scopus
  43. K. M. Habbab, D. R. Moles, and S. R. Porter, “Potential oral manifestations of cardiovascular drugs,” Oral Diseases, vol. 16, no. 8, pp. 769–773, 2010. View at Publisher · View at Google Scholar · View at Scopus
  44. J. Guggenheimer and P. A. Moore, “Xerostomia: etiology, recognition and treatment,” Journal of the American Dental Association, vol. 134, no. 1, pp. 61–69, 2003. View at Google Scholar · View at Scopus
  45. L. M. Wing, J. L. Reid, and D. S. Davies, “Pharmacokinetic and concentration-effect relationships of clonidine in essential hypertension,” European Journal of Clinical Pharmacology, vol. 12, no. 6, pp. 463–469, 1977. View at Google Scholar · View at Scopus
  46. J. Breidthardt, H. Schumacher, and L. Mehlburger, “Long-term (5 year) experience with transdermal clonidine in the treatment of mild to moderate hypertension,” Clinical Autonomic Research, vol. 3, no. 6, pp. 385–390, 1993. View at Google Scholar · View at Scopus
  47. W. W. Herman, J. L. Konzelman Jr., and L. M. Prisant, “New national guidelines on hypertension: a summary for dentistry,” Journal of the American Dental Association, vol. 135, no. 5, pp. 576–584, 2004. View at Google Scholar · View at Scopus
  48. J. S. Ellis, R. A. Seymour, J. G. Steele, P. Robertson, T. J. Butler, and J. M. Thomason, “Prevalence of gingival overgrowth induced by calcium channel blockers: a community-based study,” Journal of Periodontology, vol. 70, no. 1, pp. 63–67, 1999. View at Publisher · View at Google Scholar · View at Scopus
  49. G. Kaur, K. M. Verhamme, J. P. Dieleman et al., “Association between calcium channel blockers and gingival hyperplasia,” Journal of Clinical Periodontology, vol. 37, no. 7, pp. 625–630, 2010. View at Publisher · View at Google Scholar · View at Scopus
  50. T. Tagawa, H. Nakamura, and M. Murata, “Marked gingival hyperplasia induced by nifedipine,” International Journal of Oral and Maxillofacial Surgery, vol. 19, no. 2, pp. 72–73, 1990. View at Publisher · View at Google Scholar · View at Scopus
  51. L. Fattore, M. Stablein, G. Bredfeldt, T. Semla, M. Moran, and J. M. Doherty-Greenberg, “Gingival hyperplasia: a side effect of nifedipine and diltiazem,” Special Care in Dentistry, vol. 11, no. 3, pp. 107–109, 1991. View at Google Scholar · View at Scopus
  52. R. A. Seymour, “Effects of medications on the periodontal tissues in health and disease,” Periodontology 2000, vol. 40, no. 1, pp. 120–129, 2006. View at Publisher · View at Google Scholar · View at Scopus
  53. M. Mavrogiannis, J. S. Ellis, J. M. Thomason, and R. A. Seymour, “The management of drug-induced gingival overgrowth,” Journal of Clinical Periodontology, vol. 33, no. 6, pp. 434–439, 2006. View at Publisher · View at Google Scholar · View at Scopus
  54. S. G. Ciancio, “Medications' impact on oral health,” Journal of the American Dental Association, vol. 135, no. 10, pp. 1440–1480, 2004. View at Google Scholar
  55. P. Ellgehausen, P. Elsner, and G. Burg, “Drug-induced lichen planus,” Clinics in Dermatology, vol. 16, no. 3, pp. 325–332, 1998. View at Publisher · View at Google Scholar · View at Scopus
  56. B. H. Ackerman and N. Kasbekar, “Disturbances of taste and smell induced by drugs,” Pharmacotherapy, vol. 17, no. 3, pp. 482–496, 1997. View at Google Scholar · View at Scopus
  57. V. Musumeci, S. Di Salvo, B. Zappacosta, C. Zuppi, L. Colacicco, and P. Cherubini, “Salivary electrolytes in treated hypertensives at low or normal sodium diet,” Clinical and Experimental Hypertension, vol. 15, no. 2, pp. 245–256, 1993. View at Google Scholar · View at Scopus
  58. S. M. Popescu, M. Nechifor, M. Baniceru, O. Croitoru, and F. Popescu, “Effect of propranolol on mepivacaine serum concentrations in dental practice,” Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, vol. 105, no. 4, pp. e19–e23, 2008. View at Publisher · View at Google Scholar · View at Scopus
  59. J. A. Yagiela, “Adverse drug interactions in dental practice: interactions associated with vasoconstrictors part V of a series,” Journal of the American Dental Association, vol. 130, no. 5, pp. 701–709, 1999. View at Google Scholar · View at Scopus
  60. S. F. Malamed, Handbook of Dental Anesthesia, Elsevier Mosby, St Louis, Mo, USA, 5 edition, 2004.
  61. J. Little, D. Fallace, C. Miller, and N. Rhodus, Dental Management of the Medically Compromised Patient, Elsevier Mosby, St Louis, Mo, USA, 8 edition, 2013.
  62. C. L. Hatch, B. Chernow, and G. T. Terezhalmy, “Plasma catecholamine and hemodynamic responses to the placement of epinephrine-impregnated gingival retraction cord,” Oral Surgery Oral Medicine and Oral Pathology, vol. 58, no. 5, pp. 540–544, 1984. View at Google Scholar · View at Scopus
  63. M. Greenberg, M. Glick, and M. Ship, Burket's Oral Medicine, BC Decker Inc, 11 edition, 2008.
  64. D. Perloff, C. Grim, J. Flack et al., “Human blood pressure: determination by sphygmomanometry,” Circulation, vol. 88, no. 5, Part 1, p. 2460, 1993. View at Google Scholar · View at Scopus
  65. P. H. Gustavsen, A. Hoegholm, L. E. Bang, and K. S. Kristensen, “White coat hypertension is a cardiovascular risk factor: a 10-year follow-up study,” Journal of Human Hypertension, vol. 17, no. 12, pp. 811–817, 2003. View at Publisher · View at Google Scholar · View at Scopus
  66. R. M. Conroy, K. Pyorala, A. P. Fitzgerald et al., “Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project,” European Heart Journal, vol. 24, no. 11, pp. 987–1003, 2003. View at Publisher · View at Google Scholar · View at Scopus
  67. T. Sehestedt, J. Jeppesen, T. W. Hansen et al., “Risk prediction is improved by adding markers of subclinical organ damage to SCORE,” European Heart Journal, vol. 31, no. 7, pp. 883–891, 2010. View at Publisher · View at Google Scholar · View at Scopus
  68. M. Volpe, A. Battistoni, G. Tocci, E. Agabiti Rosei, A. L. Catapano, and R. Coppo, “Cardiovascular risk assessment beyond systemic coronary risk estimation: a role for organ damage markers,” Journal of Hypertension, vol. 30, pp. 1056–1064, 2012. View at Google Scholar
  69. K. Pyorala, G. De Backer, I. Graham et al., “Prevention of coronary heart disease in clinical practice: recommendations of the task force of the European society of cardiology, European atherosclerosis society and European society of hypertension,” European Heart Journal, vol. 15, no. 10, pp. 1300–1331, 1994. View at Google Scholar · View at Scopus
  70. R. B. D'Agostino Sr., R. S. Vasan, M. J. Pencina et al., “General cardiovascular risk profile for use in primary care: the framingham heart study,” Circulation, vol. 117, no. 6, pp. 743–753, 2008. View at Publisher · View at Google Scholar · View at Scopus
  71. J. Perk, G. De Backer, H. Gohlke, I. Graham, Z. Reiner, and M. Verschuren, “European guidelines on cardiovascular disease prevention in clinical practice (version 2012): the fifth joint task force of the european society of cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts) developed with the special contribution of the European association for cardiovascular prevention & rehabilitation (EACPR),” European Heart Journal, vol. 33, no. 13, pp. 1635–1701, 2012. View at Publisher · View at Google Scholar