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Management of Hypertension in Coronary Artery Disease
Management of Hypertension in Coronary Artery Disease
P. K. Goel, H. B. Chetan Kumar
Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
Address for correspondence: Dr. P. K. Goel, Department of Cardiology, Formerly Fellow Cardiac Radiology, Greenlane Hospital, Auckland,Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh - 226014, India.
Tel.: +91-(522)-2494227/91-(522)-2494228.
Phone: +91-9839015010/8004904685.
Fax: +91-522-2668078/2668017.
E-mail: pkgoel@sgpgi.ac.in
Received: 13-11-2017; Accepted: 09-12-2017
Hypertension (HTN) is a major modifiable independent risk factor for coronary artery disease (CAD) for all age, race, andsex groups. HTN initiates and accelerates the development of atherosclerosis. Sustained elevation of blood pressure (BP) canprecipitate acute coronary events by destabilizing vascular lesions. The cardiovascular risks attributed to uncontrolled HTN can bereduced by optimal BP control. Varying therapeutic goals for BP control and availability of numerous antihypertensives make themanagement of HTN in patients with CAD controversial. This article examines the pathophysiological mechanisms that link HTNwith CAD and discusses the available treatment options and therapeutic goals that are consistent with recently published AmericanCollege of Cardiology/American Heart Association guidelines for the prevention, detection, evaluation, and management of highBP in adults published in 2017.
Keywords: Coronary artery disease, guidelines, Hypertension, therapeutic goals
How to cite this article: Goel PK, Kumar HBC. Managementof hypertension in coronary artery disease. Hypertens2018;4(1): 41-47.
Source of support: Nil
Conflict of interest: None


Epidemiological studies have shown significant association ofhypertension (HTN) with coronary artery disease (CAD). HTNhas been shown to be a significant modifiable independent riskfactor for the development and progression of CAD, heart failure(HF), chronic kidney disease, and stroke. HTN not only playsa major role in the initiation of atherosclerosis leading to CADbut also persistently elevated levels lead to rapid progressionof the disease along with destabilization of vascular lesions,precipitating acute coronary events, and HF.[1] Various studieshave shown that HTN conferred a greater adjusted relativerisk of acute myocardial infarction (MI) than diabetes mellituswith national level surveys conducted in different countries inNorth America, Asia, and Africa indicating that HTN, on theone hand, has a high prevalence and, on the other hand, a lowawareness among the patient group leading to poor control.[2,3] These cardiovascular (CV) risks attributable to HTN canbe decreased significantly with optimal blood pressure (BP)control. The present article examines and discusses appropriate systolic BP (SBP) and diastolic BP (DBP) targets in patientswith established CAD, the optimal choice of antihypertensiveagents and evaluation of their efficacy in secondary prevention ofCAD among patients with stable ischemic heart disease (SIHD)and acute coronary syndrome (ACS).

Epidemiology of HTN and CAD in India

BP control remains an important strategy for reducing CV disease(CVD) mortality. The prospective urban rural epidemiology(PURE) study evaluated HTN awareness, treatment and controlin 17 countries at various stages of economic development.[4]Among the 142,042 participants, 40.8% had HTN and 46.5%were aware of the diagnosis. Among those who were aware of thediagnosis, the majority (87.5% of those who were aware) werereceiving pharmacological treatments, but only 32.5% of thosereceiving treatment were controlled. The percentages of thoseaware were 49.0% in high-income countries (HICs), 52.5%in upper middle-income countries (UMICs), 43.6% in lowermiddle-income countries (LMICs), and 40.8% in lower income countries (LICs) and those who were treated were 46.7% inHICs, 48.3% in UMICs, 36.9% in LMICs, and 31.7% in LICs,indicating significantly decreased awareness (P < 0.001) andtreatment in LICs (P < 0.001) compared with all other countries.Thus, overall, 46.5% of participants with HTN were aware of thediagnosis, with BP control observed among 32.5% of those beingtreated.

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In India, there are only a limited number of studies thathave reported changes in HTN prevalence over time. Anchalaet al. showed that the prevalence of HTN was 33% in urban and25% in rural Indians with awareness of hypertensive status in25% of rural and 42% of urban Indians, respectively. Only 25%of rural and 38% of urban Indians were being treated for HTNwith 10% of rural and 20% of urban hypertensive populationhaving their BP under control.[5] Ahlawat et al. reported changesin the prevalence of various CV risk factors in Chandigarh(North India) over a 30-year period with age- and sex-adjustedprevalence of HTN increasing from 27% in 1968 to 45% in 1997.A study was done in Vellore (South India) in rural and urbanpopulations in two time zones between 1991-1994 and 2010-2012 to assess changes in the prevalence of CV risk factors.[6]It was observed that age-adjusted prevalence of HTN in ruralpopulation increased in men from 8% to 17% and in womenfrom 7% to 12%, while in urban populations the increase inmen was from 20% to 27% and in women from 17% to 22%.Thus, a gradual increase in the prevalence of HTN over time isobserved.[6]

The number of studies evaluating the prevalence of knownCAD in India is also limited. The prevalence of CAD in theIndian Migration Study was 1.45%, in India Heart Watch was2.55%, and in PURE study was 2.04%.[4,6] CAD prevalence inthese studies varies from 2% to 4% and may represent a morerealistic prevalence of CAD in the general population in India.A systematic review of studies on the prevalence, risk factors,treatments, and outcomes of CAD in Indians showed that CADprevalence was 2.5%-12.6% in urban areas and 1.4%-4.6%in rural areas with overall prevalence of HTN between 13.1and 36.9% in these patients.[7] The prevalence of HTN amongpatients with ST-elevation MI (STEMI) is 65.2% and amongthose with non-STEMI (NSTEMI) is 79.2% according to datafrom ACTION registry and National CV Data Registry witha gradual increase in the prevalence of ACS observed withadvancing age.[8]

Mechanisms of HTN and CAD

Several pathophysiological mechanisms contribute to BPelevation and subsequent target organ damage, includingCAD.[1] These mechanisms include as follows:
  1. Activation of sympathetic nervous system
  2. Activation of the renin-angiotensin-aldosterone system
  3. Inhibition of the cardiac natriuretic peptide system
  4. Deficiencies in the release or activity of vasodilators such asnitric oxide and prostacyclin
  5. Increased expression of inflammatory cytokines and growthfactors in the arterial tree resulting in increased vascularstiffness and endothelial dysfunction.

The complex interaction of these neurohumoral pathwayswith genetic, demographic, and environmental factors (suchas increased psychosocial stress and excessive dietary intake ofsodium along with inadequate intake of potassium and calcium)determines the development of HTN and related CAD.

Concomitant metabolic disorders such as diabetes mellitus,insulin resistance, and obesity also lead to the production ofvasoactive cytokines that promote inflammation, endothelialdysfunction, and increased oxidative stress in the blood vessels,contributing to an increase in both BP and CVD risk.

New Definition of HTN

The recent American College of Cardiology (ACC)/AmericanHeart Association (AHA) guidelines for prevention, detection,evaluation, and management of high BP in adults (2017)categorized BP into four levels on the basis of average BPmeasured in a health-care setting (office pressures):[9]
  1. Normal
  2. Elevated
  3. Stage 1 HTN
  4. Stage 2 HTN.

Categories of BP in adults [Table 1].
This new categorization differs from that recommended inthe JNC 7 report, with Stage 1 HTN now being defined as anSBP of 130-139 or a DBP of 80-89 mmHg, and Stage 2 HTNcorresponding to Stages 1 and 2 in the JNC 7 report.[10]

The recent ESC/EHS guidelines for HTN 2018 havecategorized HTN into the following categories:
  1. Normal
  2. High normal
  3. Grade 1 HTN
  4. Grade 2 HTN
  5. Grade 3 HTN [Table 2].

BP Threshold and Goals for Patients With HTN and CAD

Numerous randomized control trials (RCTs) in HTN associatedwith CAD have yielded conflicting results regarding the optimalBP targets. In summary, these trials have demonstrated thatreduction of SBP to 130 mmHg may not provide additional target organ protection compared to SBP levels between 130and 140 mmHg. The results of two major trials, INVEST andONTARGET showed that an SBP between 130 and 139 mmHgprovided significant CV benefit compared to an SBP of 130mmHg. There was also a tendency for an increased mortalityat SBP of 130 mmHg and DBP < 70 mmHg attributed to the"J-curve" phenomenon.[11,12]

Table 1: Variations in BP
Management of Hypertension in Coronary Artery Disease

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Table 2: Parametric analysis of BP
Management of Hypertension in Coronary Artery Disease
DBP: Diastolic blood pressure, SBP: Systolic blood pressure, HTN: Hypertension

RCTs have also shown that SBP of 130 mmHg significantlyimproves cerebrovascular outcomes (stroke) with no significantbenefits in CAD. This might be explained by the possibleimpairment in autoregulatory mechanisms in CAD which mightbe preserved in cerebral vasculature.

On the contrary, the SPRINT study showed that amongpatients without diabetes, who are at high risk for CVevents, targeting an SBP of < 120 mmHg, as compared with< 140 mmHg, resulted in lower rates of fatal and non-fatal majorCV events and death from any cause.[13] An important aspect ofSPRINT trial was that the BP was measured with an automatedmeasurement system, thus eliminating the "white coat" effect,whereas an observer measured BP was included in all othermajor RCTs.

The challenge thus remains in the unpredictability of benefitobserved in which specific group of patients and at what levels ofachieved BP. The aim is to attain a uniform level of target organprotection at the same level of achieved BP.

The recently published ACC/AHA 2017 guidelinesrecommend specific thresholds and the use of risk estimation toguide drug treatment in HTN which states that.[9]
  • Use of BP-lowering medications is recommended forsecondary prevention of recurrent CV events in patientswith clinical CVD and an average SBP of 130 mmHg orhigher or an average DBP of 80 mmHg or higher (Class ofrecommendation [COR] I, level of evidence [LOE] - SBP A,DBP C).
  • Adults with confirmed HTN and known CVD or 10-yearatherosclerotic CV disease event risk of 10% or higher, aBP target of < 130/80 mmHg is recommended (COR - I,LOE - SBP: B, DBP: C).

The yet to be published ESC/EHS guidelines for HTN 2018recommend initiation of BP-lowering medication for patientswith Grade 1 HTN in high or very high-risk patients with CVdisease and in Grade 2 and 3 HTN at any level of CV risk. Itis also recommended to initiate BP-lowering medications in patients with high-normal SBP (130-140 mmHg) in patientswith very high-risk patients with established CV disease.[14]

Non-Pharmacological Management

Studies have shown that various lifestyle behaviors such asunhealthy diet, physical inactivity, and smoking, promote thedevelopment of CAD. Therefore, modifications in lifestylewith adoption of healthy behaviors are equally important in themanagement of HTN and CAD.

These include correction of unhealthy dietary patterns,excessive consumption of alcohol, and physical inactivitywhich along with pharmacological therapy form an importantcomplementary approach in the management of high BP,thereby significantly reducing CVD risk in the population.Recent ACC/AHA guidelines 2017 recommend thefollowing non-pharmacological measures for the managementof HTN.[9]
  1. Weight loss is recommended to reduce BP in adults withelevated BP or HTN who are overweight or obese (COR - 1,LOE - A)
  2. A heart-healthy diet, such as the (dietary approaches to stopHTN) diet, that facilitates achieving a desirable weight isrecommended for adults with elevated BP or HTN (COR 1,LOE A)
  3. Sodium reduction is recommended for adults with elevatedBP or HTN (COR 1, LOE A)
  4. Potassium supplementation, preferably in dietary modification,is recommended for adults with elevated BP or HTN unlesscontraindicated by the presence of CKD or the use of drugsthat reduce potassium excretion (COR 1, LOE A)
  5. Increased physical activity with a structured exercise programis recommended for adults with elevated BP or HTN (COR1, LOE A)
  6. Adult men and women with elevated BP or HTN whocurrently consume alcohol should be advised to drink no >2and 1 standard drinks per day, respectively (COR 1, LOE A).

Pharmacological Management

Epidemiological studies have shown that elevated levels of BP inCAD cause significant morbidity and mortality in the populationand that treating HTN based on specific thresholds and tocertain goals result in improvement of CV outcomes resulting insignificant positive impact on public health.Management of HTN in Patients with SIHDThe management of HTN in patients with chronic SIHD isdirected toward the prevention of death, MI, and stroke alongwith reduction in the frequency and duration of myocardialischemia, leading to symptomatic improvement. NumerousRCTs have demonstrated the benefits of antihypertensive drugtherapy in reducing the risk of ischemic heart disease.

Pharmacological strategies for the prevention of CV eventsin these patients include beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers(ARBs), thiazide and thiazide-like diuretics, and calcium channelblockers (CCBs).

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Goel and Kumar Management of hypertension in CAD

The recommendations for the management of HTN inpatients with SIHD without HF are as follows: [Table 3].

Basis of Evidence for the Current Recommendations[9]
  1. In the SPRINT trial, aggressive treatment in patients withincreased CV risk (including MI and ACS) with reductionof SBP to < 130/80 mmHg has been shown to reduce CVDcomplications by 25% and all-cause mortality by 27%.[13]
  2. In HOPE study, after 5 years of randomized therapy in high-CVD-risk patients with normal ejection or without HF,ramipril produced a 22% reduction in MI, stroke, or CVD inhigh-risk patients compared with placebo.[15] In EUROPAtrial, after 4.2 years of therapy in patients with SIHD,perindopril reduced CVD death, MI, or cardiac arrest by 20%compared with placebo.[16]
  3. Beta-blockers are effective in preventing angina pectoris,improving exercise time until the onset of angina pectorisand reducing exercise-induced ST-segment depression. Betablockershave a compelling indication for the treatment ofSIHD which result in these drugs to be recommended as afirst-line therapy in management of HTN when it occurs inthese patients. Beta-blockers used to treat SIHDs that are alsoeffective in HTN management include carvedilol, metoprololtartrate, metoprolol succinate, bisoprolol, nadolol, propranolol,and timolol. Atenolol is not considered as effective as otherantihypertensive drugs in the treatment of HTN.[9]
  4. Dihydropyridine CCBs have similar efficacy as drugs thatdecrease BP levels and relieve angina when these are addedto beta-blockers in patients with HTN and persisting anginadespite beta-blocker therapy.[9] The ALLHAT study showedthat the primary prevention of CV events with amlodipine wasequivalent to that produced by the diuretic, chlorthalidone orthe ACEI, and lisinopril.[17]
  5. Various randomized controlled trials and meta-analysis have demonstrated that the use of beta-blockers after MI reducedall-cause mortality by 23%. This established efficacy of betablockersfor treating HTN and SIHD provides reasonableevidence for continuation of beta-blockers beyond 3 yearsafter MI.[9]
  6. Beta-blockers and CCBs are effective antihypertensive andantianginal agents. CCBs including both dihydropyridineand non-dihydropyridine agents can be used separately ortogether with beta-blockers beginning 3 years after MI inpatients with CAD who have both HTN and angina.[9]

Management of HTN in Patients with ACS

HTN is one of the major modifiable risk factors for CAD,but the impact of HTN on ACS outcomes has not been welldocumented due to the limited number of studies available onspecific BP targets in patients with either STEMI or NSTEMI/UA (Non-ST-elevation MI/unstable angina).

In patients with ACS, therapeutic BP targets have not beenestablished. Current guidelines recommend a BP target of< 140/90 mmHg which applies more to secondary preventionthan HTN management during acute phase of MI.[1] Thus,initially, it is prudent to focus on pain control and clinicalstabilization, before BP levels are specifically targeted.

The BP should be lowered gradually with emphasis to avoiddecrease in DBP to < 7 0 mmHg, which may reduce coronaryperfusion, thereby worsening ischemia.

Due to the lack of specific trials to assess lowering ofBP in patients with ACS, it becomes necessary to select theantihypertensives that have established efficacy in CV riskreduction for patients with ACS independent of their BPloweringeffects. These drugs include beta-blockers, ACEI, ARBs,and, in selected patients, aldosterone antagonists [Table 4].


β-Blockers form a cornerstone of ACS treatment due to theirability to reduce myocardial oxygen demand by decreasingheart rate and BP. β-blockers demonstrate a reduction in infarct size along with decrease in sudden death after MI dueto its antiarrhythmic effects and prevention of myocardialrupture.[1]

Table 3: Recommendations for the treatment of HTN in patients with SIHD
Management of Hypertension in Coronary Artery Disease
GDMT: Guideline-directed medical therapy, HFrEF: Heart failure with reduced ejection fraction, MI: Myocardial infarction, COR: Class of recommendation,LOE: Level of evidence, DBP: Diastolic blood pressure, SBP: Systolic blood pressure, HTN: Hypertension, SIHD: Stable ischemic heart disease, BP: Bloodpressure, ACEIs: Angiotensin-converting enzyme inhibitors, ARBs: Angiotensin receptor blockers, CCBs: Calcium channel blockers
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Table 4: Class based recommendations
Management of Hypertension in Coronary Artery Disease

It is recommended that oral beta-blockers should be startedwithin the first 24 h, in stable patients with no contraindications.Short-acting cardioselective (β1-selective) β-blockers withoutintrinsic sympathomimetic activity such as metoprolol orbisoprolol are preferred. Carvedilol, which has additional β2 andα1 adrenergic receptor blocking action, results in more effectiveBP lowering than β1-selective agents resulting in their preferencein patients with ACS and severe HTN.[1]

In patients with STEMI, due to established long-term efficacyof post-discharge β-blocker administration in various studies,these drugs are routinely prescribed at the time of discharge.


CCBs have not been found to be useful in the setting of acuteSTEMI with studies documenting increase in mortalitywith the use of rapid-release form of nifedipine in post-MI settings.[1] Numerous RCTs have also noted that nondihydropyridineagents such as diltiazem and verapamil lackclinical efficacy in early MI setting and are not recommendedfor routine use in patients with STEMI. Few RCTs suggestedefficacy for CCBs in non-ST-elevation ACS patients and sincethese trials were performed >30 years ago before the practice ofroutine beta-blocker therapy, the use of CCBs in these patients islimited. Thus, CCBs are not indicated for routine use in patientswith UA or NSTEMI.[1]

The AHA/ACC guidelines (2015) for the managementof UA and NSTEMI suggest that, in patients with persistingor recurring ischemia with contraindications to β-blockers,non-dihydropyridine CCBs (verapamil or diltiazem) may beused as an effective alternative in the presence of normal LVfunction or the absence of other contraindications.[1] The useof verapamil or diltiazem in patients who have LV dysfunctionshould be avoided, and they should not be used togetherwith β-blockers in these patients to avoid acute cardiacdecompensation.


ACEIs are indicated for most patients with ACS and are apreferred option for BP management in both STEMI andNSTEMI/UA. In STEMI, ACEIs decrease infarct size andprevent LV remodeling and dilatation, thereby improving CVoutcomes. The GISSI-3 and ISIS-4 trials demonstrated a benefitfrom early administration of ACEI, with significant reductions inmortality of 0.8% and 0.5% seen as early as within 30-day post-MI.[1] A meta-analysis from the ACEI MI Collaborative Groupincluded approximately 100,000 patients with recent onset MIfound that patients treated with ACEIs had a 7% lower mortalityrate at 30 days. The benefits of ACEIs were pronounced amongindividuals with LV dysfunction and when continued long term.Significant reduction in mortality rates by 20%-25% in longtermtrials evaluating ACEIs in these high-risk subgroups hasbeen observed.[1]


ARBs are a useful alternative to ACEI in patients withcontraindication or intolerance to an ACEI.[1] The VALIANTtrial randomized patients after acute MI with LV dysfunction orHF within 10 days to valsartan, captopril, or both.[18] After 2 yearsof follow-up, the efficacy of valsartan was found to be equal ascaptopril for reducing CV events in these high-risk patients.However, the group which received both valsartan and captoprilhad increased rate of adverse events with no improvement insurvival.

Recent studies have shown that in hypertensive patientswith compelling indications (in both ACS and SIHD), there isno difference in efficacy between ARBs and ACEIs with regardto the surrogate end point of BP and the outcomes of allcausemortality, CV mortality, MI, HF, stroke, and end-stagerenal disease with overall rates of withdrawal adverse eventssignificantly lower with ARBs than with ACEIs. In view of similarefficacy and fewer adverse events with ARBs and the risk-tobenefitanalysis in aggregate indicating that ARBs in the currentera reduce CV events, including the risk of MI, as effectively asbut more safely than ACEIs, the ARBs might be preferred overACEIs for the above indications.[19]


Thiazide and thiazide-type diuretics have a role largely in thelong-term control of HTN. In patients with ACS, diuretics areused primarily in patients with the left ventricular dysfunction,resulting in increased filling pressures, pulmonary venouscongestion, or HF. Loop diuretics are considered more effectivethan thiazide and thiazide-type diuretics and preferred in ACSpatients with HF (NYHA Class III or IV).[1]

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Systemic HTN remains an important modifiable risk factorfor CAD involved in both progressions of atherosclerosis andprecipitation of acute coronary events, leading to increasedCV morbidity and mortality. The pathophysiological linkagebetween CAD and uncontrolled HTN and the clinicalimplications of HTN on CAD have been described in variousguidelines with considerable debate existing regarding thespecific thresholds for treatment initiation and optimaltherapeutic goals beneficial in reducing CV events. Recentlypublished guidelines recommend treatment initiation at BPlevels ≥130/80 mmHg to a therapeutic BP goal to 130/80mmHg in patients with HTN and SIHD with a target BP of< 140/90 mmHg in patients with HTN and ACS. However,cautious observation is necessary while reducing the DBP< 80 mmHg due to adverse events attributed to the J curvephenomenon, leading to coronary hypoperfusion andincreased CV events. These specific targets can be achievedby effective single or sequential combination drug therapy,which includes beta-blockers, ACEIs, or ARBs, irrespective ofLV function with CCBs used as an alternative to beta-blockersor an addition to standard therapy. The aim is to achieve andmaintain target BP goal resulting in reduced morbidity andmortality associated with both CAD and HTN. It is expectedthat ESC/EHS guidelines for HTN to be published in 2018might offer more insight regarding the management of HTNin CAD patients.

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