Building on the Specialist's Antihypertensive Treatment Recommendation: It's Just the Beginning

Abstract

Patients with established cardiovascular disease are a top priority for preventive medicine. Evidence from clinical trials supports the merits of aggressive risk reduction therapies in survivors of an acute event. Improving their cardiovascular risk factor profile prolongs survival, reduces the incidence of recurrent atherosclerotic events, and improves quality of life. Blood pressure (BP) control is an essential component of cardiovascular disease secondary prevention programs; however, many patients are not receiving adequate antihypertensive therapy to meet their BP goal. By building on the specialist's discharge antihypertensive prescription, primary care physicians are ideally positioned to assume responsibility for ensuring BP goals are achieved and maintained over the long term in patients who have survived an acute event. Current hypertension management guidelines define appropriate BP goals and incorporate clear advice on how these goals can be met. BP should be lowered slowly and carefully through lifestyle modifications and pharmacologic therapy. Antihypertensive treatment should be given according to guidelines for primary prevention, although specific antihypertensive classes are indicated for initial use in post‐myocardial infarction and post‐stroke patients. In many cases, BP goal attainment will require the use of combination therapy with two or more drugs from different classes. With the availability of effective and safe antihypertensive drug therapies, including fixed‐dose combinations, a BP goal of <140/90 mm Hg should be achievable in most patients.

Cardiovascular disease (CVD) is the leading cause of death and a major cause of disability in the United States. ¹ Despite advances in the medical and surgical management of CVD, long‐term survival depends ultimately on modifying and slowing progression of the underlying atherosclerotic disease process through risk factor control.

Hypertension (sustained systolic blood pressure [SBP] of at least 140 mm Hg and/or diastolic blood pressure [DBP] of at least 90 mm Hg) is a potent and highly prevalent CVD risk factor. According to National Health and Nutrition Examination Survey (NHANES) statistics, at least 65 million adults in the United States had hypertension in 1999–2000, representing a prevalence rate of 31.3%. ² Elevated blood pressure (BP) plays a major etiologic role in the development and progression of CVD by accelerating atherogenesis and by causing degenerative changes in the endothelium and walls of large and medium arteries. ³ Through its effects on vascular beds in different target organs, hypertension contributes to the pathogenesis of ischemic heart disease, stroke, transient ischemic attack (TIA), cardiac failure, and renal failure.

The risk of death from ischemic heart disease and stroke increases continuously, linearly, and independently from usual BP levels as low as 115 mm Hg systolic and 75 mm Hg diastolic, the heightened risks being apparent in all age groups between 40 and 89 years. ⁴ At ages 40–69 years, with each 20‐mm Hg increase in usual SBP (or, approximately equivalently, 10‐mm Hg increase in usual DBP), there is a doubling of mortality from both ischemic heart disease and stroke; ⁴ lowering BP decreases these risks. In patients with SBP 140–159 mm Hg and/or DBP 90–99 mm Hg (stage 1 hypertension), estimates indicate that sustaining a 12‐mm Hg reduction in SBP over 10 years will prevent one death for every 20 patients treated. ⁵ The number‐needed‐to‐treat to prevent one death is estimated at 11 if additional risk factors are present and only nine if concomitant CVD or target organ damage is present.

Increasing numbers of patients are surviving myocardial infarction (MI) and stroke, largely due to improvements in acute management, but they are at high risk for recurrent events. Long‐term care of these individuals focuses on aggressive risk reduction therapies to improve patient survival, reduce recurrent events and the need for interventional procedures, and improve quality of life. ⁶ Lowering BP to goal levels is a vital component of such secondary CVD prevention programs. The larger the burden of risk—patients with established CVD are among those at highest risk—the more important it is to reach and maintain BP goals. ⁷ Furthermore, patients with clinical evidence of CVD may be more highly motivated than their healthy counterparts to make and maintain lifestyle changes and comply with treatment regimens. ⁸ Secondary prevention measures are also a cost‐effective way to reduce the substantial morbidity and mortality associated with CVD. ⁹

CARDIOVASCULAR RISK POST‐MI

People who survive an acute MI have a greatly increased risk of a second cardiovascular event, be it another MI, sudden cardiac death, heart failure, or stroke. ¹ Depending on gender and clinical outcome, the risk of morbidity and mortality among MI survivors is between 1.5 and 15 times higher than that of the general population. ¹ In addition, it is estimated that 18% of men and 35% of women will have another MI and 8% of men and 11% of women will have a stroke within 6 years of a first MI. ¹

A history of hypertension is an independent predictor of reinfarction. ¹⁰ Myocardial oxygen supply may be impeded by the presence of coronary artery disease in patients with hypertension. Moreover, myocardial oxygen demand is often greater among hypertensive individuals because of the increased impedance to left ventricular ejection and the frequent presence of left ventricular hypertrophy. Lowering SBP and DBP decreases ischemia and prevents cardiovascular events in patients with coronary artery disease in part by decreasing myocardial oxygen demand.

CARDIOVASCULAR RISK POST‐STROKE

As with post‐MI patients, post‐stroke patients have a greatly increased risk of a recurrent event. Of the 700,000 strokes that occur in the United States each year, about 200,000 are recurrent attacks. ¹ The 5‐ and 10‐year risk of a first recurrent stroke in the Perth Community Stroke Study ¹² was 32% and 43%, respectively, among patients with acute stroke and, of those who survived to 10 years, about one in seven required institutional care and almost one half were disabled. ¹¹ Furthermore, the risk of death at 10 years was 79%, the most common cause being cardiovascular disease. Patients who survive an acute stroke, therefore, have an ongoing burden of fatal vascular disease, recurrent stroke, and subsequent disability, which emphasizes the importance of long‐term control of cardiovascular risk factors, including BP.

The benefits of BP control in preventing first strokes are well established. ¹³ Individuals whose BP is <120/80 mm Hg have about half the lifetime risk of stroke vs. individuals with hypertension. ¹ A meta‐analysis of more than 40 randomized controlled trials involving over 188,000 individuals and approximately 6800 events indicates that the benefits of BP lowering for stroke risk reduction are broadly consistent across a range of different population subgroups. ¹⁴ Greater BP reductions appeared to be associated with greater reductions in risk, and initiating and maintaining BP control was more important than the selection of a specific initial agent. ¹⁴

The very compelling evidence that first stroke can be averted by BP control is now substantiated for recurrent stroke. Several clinical studies have provided reassurance that BP lowering is safe and reduces the risk of recurrent stroke in people with cerebrovascular disease, including the Post‐Stroke Antihypertensive Treatment Study (PATS), ¹⁵ the United Kingdom Transient Ischemic Attack (UK‐TIA) trial, ¹⁶ the Perindopril Protection against Recurrent Stroke Study (PROGRESS), ¹⁷ the Heart Outcomes Prevention Evaluation (HOPE), ¹⁸ and the Morbidity and Mortality After Stroke—Eprosartan Compared with Nitrendipine for Secondary Prevention (MOSES) study. ¹⁹ A systematic review of seven randomized controlled trials investigating the effect of lowering BP on recurrent vascular events over 2–5 years in patients with prior stroke or TIA showed that lowering BP with a variety of antihypertensive agents reduced the risk of fatal stroke by 24%, nonfatal stroke by 21%, MI by 21%, and total vascular events by 21% (Table I). ²⁰ The reduction in stroke was significantly related to the magnitude of the SBP reduction.

Table I.

Effect of Lowering Blood Pressure on Stroke, Myocardial Infarction, All Vascular Events, and Death

Outcome	No. of Trials	Events (n)	Subjects (n)	Rate in Control Group (%)	OR	95% CI	p Value	Heterogeneity (p Value)
All stroke	7	1577	15,527	11.5	0.76	0.63–0.92	0.005	0.01
Fatal	7	329	15,527	2.4	0.76	0.56–1.03	0.08	0.16
Nonfatal	7	1268	15,527	9.2	0.79	0.65–0.95	0.01	0.042
All myocardial infarction	6	555	15,428	4.0	0.79	0.63–0.98	0.03	0.19
All vascular events	6	2225	15,428	16.0	0.79	0.66–0.95	0.01	0.002
Vascular death	7	852	15,527	5.9	0.86	0.70–1.06	0.16	0.066
All death	7	1427	15,527	9.6	0.91	0.79–1.05	0.18	0.17
Odds ratio (OR) and 95% confidence intervals (CI) were determined using a random effects model. Data from a systematic review of seven randomized controlled trials over 2–5 years in patients with prior stroke or transient ischemic attack. Reproduced with permission from Stroke. 2003;34:2741–2748. 20

HYPERTENSION CONTROL IN SECONDARY PREVENTION

Despite its importance as a major risk factor for recurrent cardiovascular events, rates of BP control in secondary prevention are poor. For example, 53% of stroke and MI survivors with previously diagnosed hypertension participating in NHANES III ²¹ (1988–1994) had uncontrolled BP (i.e., >140/90 mm Hg) during follow‐up (Figure 1). An additional 11% of survivors had hypertension that was previously undetected. The situation is similar in Europe. In the first European Action on Secondary Prevention by Intervention to Reduce Events survey (EUROASPIRE; ²² 1995–1996), 53% of patients had uncontrolled BP (≥140/90 mm Hg) 6 months after hospitalization for coronary heart disease. BP control rates were found to be no better in a second survey conducted 4 years later (EUROASPIRE II; 1999–2000). ²³ Suboptimal BP goal attainment rates in secondary prevention among post‐MI and post‐stroke patients in general practice have been shown in many other studies. ²⁴ , ²⁵ , ²⁶ , ²⁷

Figure 1.

Distribution of systolic and diastolic blood pressure in survivors of my o car dial infarction and stroke in the Third National Health and Nutrition Survey (NHANES) population. The grey and black bars, respectively, represent levels below and above 140/90 mm Hg, the cutoff value for defining inadequate control. Reproduced with permission from Arch Intern Med. 2001;161:1621–1628. ²¹

It is possible that patients with uncontrolled BP several months after an acute event had uncontrolled BP at the time of discharge. In an observational survey conducted in France (the PREVENIR study ²⁸ ), the medical records of patients who were admitted for a MI or unstable angina and survived were studied. At the time of hospital discharge, 33% of patients had uncontrolled BP (≥140/90 mm Hg). However, the authors speculated that discharge BP was likely to be an underestimate of follow‐up BP because of prolonged bed rest and enhanced surveillance during hospitalization. If so, this reinforces the need for primary care physicians (PCPs), through regular follow‐up appointments, to maintain continuity in patient care between management of the acute event by specialists and long‐term cardiovascular risk factor control, including BP control, following hospital discharge.

Patients at high risk for a recurrent cardiovascular event who do not have their antihypertensive medication titrated to achieve and maintain goal BP remain exposed to the cardiovascular risks associated with elevated BP. The reductions in secondary cardiovascular events reported in clinical trials will only be realized when BP is lowered to the levels specified in hypertension management guidelines, which are based on the results of controlled outcomes trials. Thus, there is a clear opportunity for PCPs, through their vigilance, to improve the prognosis of post‐MI and post‐stroke patients by long‐term BP control to goals specified in guidelines.

General Considerations

The PCP should accept the responsibility of achieving and maintaining BP goals in patients with established CVD who have survived an acute event by building on the discharge antihypertensive regimen. Treatment should be given according to hypertension management guidelines for primary prevention. The most influential guidelines in the United States are currently those contained in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). ²⁹ In addition, guidelines published by the International Society on Hypertension in Blacks (ISHIB) ³⁰ provide realistic and practical recommendations regarding the care of one of the highest risk hypertensive populations, i.e., African Americans. The World Health Organization/International Society of Hypertension (WHO/ISH) have also published a joint statement providing guidance for the treatment of people with elevated BP. ⁷

BP Targets

BP target levels among the various current national and international hypertension management guidelines are largely consistent. The JNC 7 report recommends a SBP target of <140 mm Hg and a DBP target of <90 mm Hg for individuals with uncomplicated hypertension (i.e., no diabetes or evidence of target organ damage, no history of a cardiovascular event, and at low or moderate risk for coronary heart disease). ²⁹ Lower targets of <130 mm Hg SBP and <80 mm Hg DBP are recommended for individuals with diabetes or chronic kidney disease due to their higher‐risk status. The ISHIB expert consensus on hypertension management specifies similar BP target levels for African Americans: <140 mm Hg SBP and <90 mm Hg DBP for individuals with uncomplicated hypertension and <130/80 mm Hg for patients with diabetes or nondiabetic renal disease characterized by proteinuria of >1 g/d. ³⁰

Precise BP goals for optimal secondary prevention have not yet been established. Targets lower than 130/80 mm Hg might be desirable, as BP reductions to levels below or beyond traditional thresholds appeared to confer proportionately greater benefit with minimal additional risk, as observed in the Hypertension Optimal Treatment (HOT) study, ³¹ HOPE, ³² and PROGRESS. ¹⁷ The ISHIB consensus statement proposes that a BP target <140/90 mm Hg (e.g., <130/80 mm Hg) may be preferred for patients with a history of a cardiovascular event; stroke or TIA; evidence of target organ damage, including microalbuminuria; coronary heart disease; or high risk of coronary heart disease. ³⁰ Prior MI, or prior stroke or TIA, are classified as associated clinical conditions in the WHO/ISH guidelines. ⁷ Hypertensive patients with an associated clinical condition are stratified as at “high risk'” for a cardiovascular event; a goal of <130/80 mm Hg is deemed appropriate for patients in this risk band.

Treatment Recommendations

The JNC 7 report incorporates a simple, practical, evidence‐based algorithm that provides clear advice on the steps needed to achieve BP goals in the general population of patients with hypertension (Figure 2). ²⁹ A corresponding algorithm relating specifically to the treatment of African Americans is included in the ISHIB consensus statement (Figure 3). ³⁰ Both schemata encourage all patients to follow healthy lifestyles as a first step in reducing BP. Effective lifestyle modifications include weight reduction in overweight or obese individuals, adoption of the Dietary Approaches to Stop Hypertension (DASH) diet, restriction of sodium and alcohol intake, increased physical activity, and smoking cessation. Combining multiple lifestyle changes is associated with greater BP reductions and, presumably, lower cardiovascular risk. ³³

Figure 2.

Clinical algorithm for achieving target blood pressure, as recommended in the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). SBP=systolic blood pressure; DBP=diastolic blood pressure; ACEl=angiotensin‐converting enzyme inhibitor; ARB=angiotensin receptor blocker; BB=β blacker; CCB=calcium channel blocker. Reproduced with permission from JAMA. 2003;289:2560–2572. ²⁹

Figure 3.

Clinical algorithm for achieving target blood pressure (BP) in African‐American patients, as recommended by the Hypertension in African Americans Working Group of the International Society on Hypertension in Blacks. RAS=renin‐angiotensin system; *initiate monotherapy at usually recommended doses with a diuretic, β blocker, calcium channel blocker (CCB), angiotensin‐converting enzyme (ACE) inhibitor, or angiotensin receptor blocker (ARB); finitiate low‐dose combination therapy with an ACE inhibitor/diuretic, ARB/diuretic, β‐blocker/diuretic, or ACE inhibitor/CCB combination. Reproduced with permission from Arch Intern Med. 2003;163:525–541. ³⁰

If therapeutic lifestyle changes are insufficient to lower BP to optimal levels, initiation of pharmacologic treatment is appropriate. Previous MI and stroke have both been identified as compelling high‐risk indications for prescribing specific classes of antihypertensive agents, based on the results of controlled clinical trials (Table II). ²⁹

Table II.

Clinical Trial and Guideline Basis for Compelling Indications for Individual Drug Classes in the Treatment of Hypertension

	Recommended Drugs
Compelling Indication	Diuretic	β Blocker	ACEI	ARB	CCB	Aldosterone Antagonist	Clinical Trial Basis
Heart failure	•	•	•	•		•	ACC/AHA Heart Failure Guideline, 41 MERIT‐HF, 48 COPERNICUS, 49 CIBIS, 47 SOLVD, 61 AIRE, 42 TRACE, 43 Val‐HeFT, 44 RALES, 50 CHARM 45
Post‐myocardial infarction		•	•			•	ACC/AHA Post‐Myocardial Infarction Guideline, 6 BHAT, 34 SAVE, 62 Capricorn, 63 EPHESUS 37
High coronary disease risk	•	•	•		•		ALLHAT, 64 HOPE, 32 ANBP2, 65 LIFE, 57 CONVINCE, 55 EUROPA, 66 INVEST 67
Recurrent stroke prevention	•		•		•		PROGRESS 17
ACEI=angiotensin‐converting enzyme inhibitor; ARB=angiotensin receptor blocker; CCB=calcium channel blocker; ACC/AHA=American College of Cardiology/American Heart Association; MERIT‐HF=Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure; Post‐myocardial=Carvedilol Prospective Randomized Cumulative Survival trial; CIBIS=Cardiac Insufficiency Bisoprolol Study; SOLVD=Studies of Left Ventricular Dysfunction; AIRE=Acute Infarction Ramipril Efficacy trial; TRACE=Trandolapril Cardiac Evaluation; Val‐HeFT=Valsartan Heart Failure Trial; RALES=Randomized Aldactone Evaluation Study; CHARM=Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity; BHAT=Beta‐Blocker Heart Attack Trial; SAVE=Survival and Ventricular Enlargement trial; Capricorn=Carvedilol Post‐Infarct Survival Control in Left Ventricular Dysfunction study; EPHESUS=Eplerenone Post‐Acute Myocardial Infarction Heart Failure Efficacy and Survival Study; ALLHAT=Antihypertensive and Lipid‐Lowering Treatment to Prevent Heart Attack Trial; HOPE=Heart Outcomes Prevention Evaluation; ANBP2=The Second Australian National Blood Pressure Study; LIFE=Losartan Intervention For Endpoint Reduction in Hypertension study; CONVINCE=Controlled Onset Verapamil Investigation of Cardiovascular End Points; EUROPA=The European Trial on Reduction of Cardiac Events with Perindopril in Stable Coronary Artery Disease; INVEST=International Verapamil‐Trandolapril Study; PROGRESS=Perindopril Protection Against Recurrent Stroke Study From the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). Reproduced with permission from JAMA. 2003;289:2560–2572. 29

Lowering BP in Post‐MI Patients. The overall objectives of medical therapy in patients who have already sustained an MI are to avert recurrent cardiovascular events, prevent premature disability and death, reduce myocardial ischemia, and alleviate angina symptoms. ²⁹ Lowering BP with appropriate agents represents one of the most important strategies through which cardiovascular risk reduction can be achieved.

Previous MI is a compelling indication for antihypertensive treatment with a β blocker, angiotensin‐converting enzyme (ACE) inhibitor, or aldosterone antagonist (Table II). ³⁴ , ³⁵ , ³⁶ , ³⁷ Thus, an agent from any of these classes should be prescribed as initial therapy. Although angiotensin receptor blockers (ARBs) may also have a place in the management of hypertensive post‐MI patients, their specific value in this patient population requires further clarification. ³⁸ , ³⁹ , ⁴⁰

ACE inhibitors are the preferred antihypertensive drug class in post‐MI patients with coexisting heart failure. ⁴¹ , ⁴² , ⁴³ ARBs may be a useful alternative, especially in patients who are unable to tolerate ACE inhibitors due to treatment‐related cough. ⁴⁴ , ⁴⁵ , ⁴⁶ Beta blockers, diuretics, and aldosterone antagonists are also recommended for BP management in patients with heart failure. ²⁹ , ³⁰ , ⁴⁷ , ⁴⁸ , ⁴⁹ , ⁵⁰

Lowering BP in Patients With Prior Stroke or TIA.

Initiating antihypertensive treatment during the acute phase of stroke remains controversial. There are concerns that a sudden decrease in BP will impair cerebral perfusion in patients with known cerebrovascular disease and worsen outcome from the acute event. ⁵¹ , ⁵² However, preexisting stroke is not a contraindication to controlling BP over the long term and it can be started when the patient is stable (i.e., at least 1 week after the onset of stroke).

If the patient is stable and was not discharged on antihypertensive therapy by the neurologist, it should be initiated as soon as possible unless contraindicated. In the absence of evidence‐based guidelines for medical management of hypertension in post‐stroke patients, utilization of JNC 7 recommendations and goals seems reasonable (Figure 2). ²⁹ These guidelines identify previous stroke as a compelling indication for initial treatment with an ACE inhibitor or a thiazide diuretic. ¹⁷ , ²⁹ It is possible that future guidelines may extend this recommendation to ARBs, in light of recent data from the MOSES trial. ¹⁹ Hypertensive stroke patients treated with eprosartan experienced significantly fewer events (composite of total mortality and all cardiovascular and cerebrovascular events) than nitrendipine for an equivalent reduction in BP. ¹⁹

Combination Therapy.

Based on clinical trial experience, ³¹ , ⁵³ , ⁵⁴ , ⁵⁵ , ⁵⁶ , ⁵⁷ contemporary hypertension management guidelines acknowledge that most patients will require at least two antihypertensive agents from different classes to attain target BR ¹ , ²⁹ , ³⁰ , ⁵⁸ For example, in the Antihypertensive and Lipid‐Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), ⁵³ which involved patients 55 years of age and older with hypertension plus at least one other coronary heart disease risk factor, 63% of patients controlled to <140/90 mm Hg at 5 years were taking two or more antihypertensive agents.

The advice in JNC 7 pertaining to the use of combination therapy for lowering BP is valid for post‐MI and post‐stroke patients as well as the general population. For patients not achieving BP goal on initial treatment (i.e., the drug for the compelling indication), a second drug from another class should be added, either as a separate prescription or a fixed‐dose combination. Rational antihypertensive drug combinations should be based on their ability to produce additive BP reductions (through complementary mechanisms of action) and to minimize the incidence of dose‐dependent side effects.

Both JNC 7 and the ISHIB statement advise physicians to consider initiating antihypertensive treatment with two drugs if BP exceeds certain limits at presentation. However, this practice may not be appropriate for patients with established CVD in whom BP should be lowered more gradually.

Follow‐Up

BP reduction should be conducted in a careful and controlled manner following a cardiovascular event. Reaching BP goal within a 3‐ to 6‐month time frame is a reasonable expectation. After initiation of antihypertensive therapy, follow‐up for BP monitoring and adjustment of medications in the setting of secondary prevention should be consistent with JNC 7 guidelines. ²⁹ For the general population, follow‐up visits should occur at least once a month until the BP goal is reached and at 3‐ to 6‐month intervals thereafter. However, more frequent follow‐up is recommended for patients with complicating comorbidities, including those with a previous event.

Follow‐up visits should include evaluation and management of other CVD risk factors, such as smoking, dyslipidemia, diabetes, and overweight/obesity. Low‐dose aspirin can be initiated, but only when BP is controlled, due to the increased risk of hemorrhagic stroke among patients with uncontrolled hypertension. ⁵⁹ Follow‐up visits also provide an opportunity for physicians to reinforce the benefits of following a healthy lifestyle and to educate patients on the progressive nature of atherosclerotic disease, their level of risk, and the need to take drugs for the rest of their lives.

CONCLUSIONS

Cardiovascular disease is a leading cause of mortality in the United States, despite advances in the understanding of underlying risk factors and drug therapy options and the development of practice guidelines for secondary prevention. Many patients fail to meet their clinical treatment goals because of low compliance, underuse of combination therapy, and comorbidities that require modifications to management plans.

Because of the continuity of the circulation, individuals with atherosclerosis in the cerebral (i.e., post‐stroke or TIA patients) or coronary (i.e., post‐MI patients) arteries are at high risk for events in other vascular beds. Even though these patients are identified within the health care system, long‐term treatment to manage their cardiovascular risk factors, such as hypertension, to goal is often unsatisfactory.

Compelling evidence exists that lowering BP in patients with documented CVD decreases the risk of recurrent cardiovascular events. Since hypertension has no significant early symptoms that may prompt patients to seek treatment, it is usually only detected during clinician visits for routine health checkups or for other medical problems. Consequently, some individuals with elevated BP remain unaware of their condition for many years, during which time subclinical target organ damage may develop. In some cases, hypertension is only diagnosed after admission to a specialist unit following an acute coronary or cerebrovascular event.

Hospitalization may be an ideal time for the responsible physician to review a patient's cardiovascular risk factor profile and devise an effective secondary prevention strategy to manage these risk factors. In‐hospital initiation of cardiac therapy improves patient compliance ⁶⁰ and provides guidance to the PCP on secondary prevention. Thereafter, the responsibility lies with the PCP for long‐term care of the post‐MI or post‐stroke patient to ensure that they are attaining and maintaining the goals set out in management guidelines.

BP control should be assiduously pursued as in any CVD secondary prevention strategy. It should be lowered gradually through therapeutic lifestyle measures and pharmacologic intervention and to a goal of at least 140/90 mm Hg. Specific classes of antihypertensive agents are recommended as initial therapy for patients with concomitant compelling indications, such as those with prior MI or stroke, based on the benefits observed in clinical outcome trials. Increased use of antihypertensive combination therapy, either as separate prescriptions or as fixed combinations, will help patients achieve and sustain their target BR Hypertension should not be managed in isolation, however, but should represent one component of a strategy aimed at improving the patient's overall cardiovascular risk profile.

Harmonization and communication between specialist physicians, such as cardiologists and neurologists, and PCPs, who are involved in the day‐to‐day care of patients, will improve hypertension treatment in patients with a prior event. Attaining and maintaining BP goals in these patients will be an important factor in prolonging their survival and preventing premature disability.

Disclosure:

Editorial assistance for the development of this manuscript was provided by Elaine Griffin, PhD, Envision Pharma, with the financial support of the Bristol‐Myers Squibb ISanofi‐Synthelabo Partnership. Dr. Saunders provides speaking and consulting services for Abbott Laboratories, Bristol‐Myers Squibb Co., Novartis, Pfizer Inc., Sanofi‐Aventis, and Wyeth/Monarch.