Close Encounter - Hypertension & IHD

7/28/2019 Close Encounter - Hypertension & IHD

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Vol No 002Cardiology

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Case study on Ischemic Heart Disease & Hypertension


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CLOSE ENCOUNTER: ISCHEMIC HEART

DISEASE & HYPERTENSION

A 42 years old, obese male patient, working as a senior

executive in a bank, was brought to the emergency department

in a confused state, following complaints of severe headache,

slight neck stiffness and blurring of vision. There were no other

complaints.

Patient was apparently alright till about a year ago, when he

started experiencing sub-occipital headaches, which was

aggravated by noise and relieved on taking medication. In the

past few weeks, the intensity of the episodes had increased.

There were no complaints of fever, shortness of breath, chest

discomfort or seizures.

On taking further history, it was found that patient was a known

hypertensive stabilized on Amlodipine (5mg OD) since the last

10 years.

Family historyrevealed that his father deceased at the age

of 55 yrs due to AMI and mother is a known

hypertensive/diabetic with CAD and has undergone PTCA

5 years ago for single vessel disease (LAD).

Personal historyrevealed that he is a chronic smoker (10

cigarettes/day for the last 20 years) and occasional

alcoholic. He also had long working hours at office for the

past one month.


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Physical examination showed the following:

Patient was confused and disoriented

Temperature: normal

P-96/min

BP-220/110 mmHg

R/R-16/min

CVS: S1 S2 normal, JVP not raised and there was no pedal

edema RS: Air entry bilaterally equal, no basal rales

Eye examination revealed

increased intra ocular

pressure and fundoscopic

examination revealed

arteriolar vasoconstriction,cotton wool spots and

papilloedema

1. What is the probable diagnosis in this case?

a. Accelerated hypertension

b. Migrainec. Meningitis

d. Tension headache

Answer is a) Accelerated hypertension

The patient in this case is a known hypertensive and has

presented with a very high blood pressure of 220/110 mmHg. In


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addition he is disoriented, has headache and blurring of vision.

Fundoscopic examination has revealed papilloedema and other

signs of hypertensive retinopathy. All these findings aresuggestive of an accelerated hypertension. This disorder affects

about 1% of people with high blood pressure, including both

children and adults.

People at risk for developing malignant hypertension are:

Young hypertensives

Women with toxemia of pregnancy, and

Patients with existing kidney disorders or collagen vascular

disorders

Malignant hypertension is a medical emergency. Multiple organs

of the body, including the brain, eyes, blood vessels, heart, and

kidneys are involved and may sustain damage.

Migraine is characterized by episodic recurrent headaches, may

be unilateral, often associated with nausea, vomiting, or

photophobia. Aura may or may not be present. It is more

common in women and a family history is usually present. This is

not suggestive in this patient.

Headache due to meningitis is often accompanied by high grade

fever, vomiting, and stiff neck. Diagnosis is confirmed by CSFexamination. These features are not seen in this patient.

Tension type headache is usually generalized and aura is absent.

It occurs commonly in patients subjected to stress, anxiety or

depression. This is not the case in this patient.


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2.The findings in a patient with hypertensive retinopathy

are:

a) Arteriolar vasoconstriction

b) Cotton wool spots

c) Flame shaped hemorrhages

d) All of the above.

Answer is d) All of the above.

Vascular changes in the fundusref lect both hypertensive

retinopathy and arteriosclerotic

retinopathy. The two processes

first induce narrowing of the

arteriolar lumen (grade 1) and

then sclerosis of the adventitia

and /or thickening of the

arteriolar wall, visible as arteriovenous nicking (grade2).

Progressive hypertension induces rupture of small vessels, seen

as hemorrhage and exudates (grade3) and eventually

Grade 1

Grade 2


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papilledema (grade4). The grade3 and

4 changes are clearly indicative of an

accelerated-malignant form ofhypertension, whereas the lesser

changes can be correlated with the

risk of coronary disease.

Laboratory investigations revealed the following:

a) Electrocardiography (ECG) - No evidence of ST

depression or elevation.

b) 2 D Echo showed mild left ventricular hypertrophy, LV2

mass index was raised 140g/m , and ejection fraction

(EF) was adequate

c) Brain MRI showed micro hemorrhages

d) Electrolytes were normal; BUN and serum creatinine

levels were elevated.

e) Plasma and urinary catecholamine levels for

pheochromocytoma were negative.

f) CXR was normal.

g) Lipid profile Serum cholesterol: 170mg/dL

Serum Triglyceride: 150mg/dL

HDL cholesterol: 45mg/dL

LDL cholesterol: 120mg/dL

h) Random blood sugar was 110mg%

Grade 3&4Case history contd..


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3. The following medications can be used to control BP

in this patient, except

a) Sodium Nitroprusside

b) Nitroglycerin

c) Labetalol

d) Diazepam

Answer is d) Diazepam.

Sodium Nitroprusside is the first-line medication forhypertensive encephalopathy. It decreases systemic vascular

resistance via direct dilatation of arterioles and veins. It is used in

the dose of 0.5-1 mcg/kg/min IV infusion, titrate to desired BP.

Nitroglycerin causes arteriolar dilation and venodilation. It is

used in emergencies involving myocardial ischemia due to the

dilatory effects of nitroglycerin on coronary arteries. It is used inthe dose of 5-300 mcg/min IV infusion, titrate to desired BP.

Labetalol is a competitive and selective alpha1-blocker and

nonselective beta-blocker with predominantly beta effects at

low doses. Onset of action is 5 min, with half-life of 5.5 h. It

provides a steady, consistent drop in BP without compromising

cerebral blood flow. It is usually started with the dose of 20 mgIV bolus, then administered as 2 mg/min IV infusion, titrate to

desired BP; not to exceed 300 mg.

Diazepam is not an antihypertensive. It has been used in this

patient to relieve the anxiety and as a prophylactic to prevent

seizures.


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Case history cont

Patient was managed with IV Nitroprusside and IV Diazepam.

His BP was controlled and later on he was shifted to his routineoral antihypertensive medication. On discharge he was advised,

regular follow up, dietary restrictions (low salt and low fat diet),

cessation of smoking and avoidance of alcohol.

After one year, on the above treatment, the patient returned

with complaints of substernal chest pain, nausea and vomiting.

The pain was burning and stabbing in character and radiated tothe jaw. On examination, his BP was 150/100mm Hg, P-80/min.

An emergency ECG revealed ST segment depression in lead II

and he was diagnosed to have angina pectoris.

4. What are the risk factors for angina?

a) Hypertension

b) Elevated lipid levels

c) Smoking

d) All of the above

Answer is d) All of the above

Angina pectoris is a disorder of multi-factorial etiology. Thefollowing are some of the risk factors for the development of

angina:

Male gender

Obesity

Hypertension


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Hyperlipidemia

Smoking

Diabetes Stress

Sedentary life style

In this patient, obesity, hypertension, male gender, smoker,

stress and hypercholesterolemia were the prominent risk

factors.

Case history contd...

The situation was managed with administration of sublingual

Nitroglycerine and Aspirin. This episode of cardiovascular

involvement was uneventful.

On discharge, the patient's investigations revealed thefollowing

Lipid profile

Total cholesterol: 180 mg/dl

Serum TG: 160mg/dl

HDL 40mg/dl

LDL cholesterol: 150mg/dl 2D Echo revealed moderate LVH with LV mass index of

2160g/m and development of NYHA Grade I CCF. LVEF

was 50%.

CT scan (brain) was normal

ECG: WNL


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5. What is the LDL goal that should be achieved in this

patient according to ATP-III recommendations?

a) < 100 mg/dlb) < 130 mg/dl

c) < 160 mg/dl

d) None of the above

Since the patient has a high risk of coronary heart disease, hence

the answer is a) < 100 mg/dl.

The LDL Cholesterol Goals and cut-off points for Therapeutic

Lifestyle Changes (TLC) and Drug Therapy in Different Risk

Categories according to the ATP III recommendations are;

* Some authorities recommend use of LDL-lowering drugs in this category if an LDL

cholesterol 130 mg/dLEquivalents (10-year (100-129 mg/dL:risk >20%) 100 mg/dL drug optional)*

2+ Risk Factors 10-year risk 10-20%:(10-year risk less >130 mg/dLthan or equal to 20%) 130 mg/dL ---------------------

10-year risk 160 mg/dL0-1 Risk Factor 160 mg/dL >190 mg/dL

(160-189 mg/dL: LDLlowering drug optional)


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fibrate. Clinical judgment also may call for deferring drug therapy in this subcategory.

Almost all people with 0-1 risk factor have a 10-year risk


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The patients BP was 120/70 mmHg, PR was 90/min.

Thrombolytic treatment was undertaken, and heparin and

antiplatelet agents were started.

A 2D Echo revealed an EF of 40%, indicating impaired cardiac

function, progression to Grade II CCF, LVH and regional wall

motion abnormality localized to the inferior wall.

Post MI, patient's heart rate remained elevated and he was found

to be anxious. Since Echo revealed impaired cardiac function,

the physician hence decided to change his antihypertensive

medication to a combination of Bisoprolol 2.5mg and

Hydrochlorothiazide 6.25mg per day.

At the time of discharge, his BP was stabilized at 126/88mm Hg.

He was asked to continue statins for hyperlipidemia and Aspirin

75mg/day.He was strictly advised lifestyle and dietarymodifications, and cessation of smoking/alcohol.

The patient returned for follow up after 3 months. The blood

pressure was maintained (128/84 mmHg), cholesterol levels

were under control and LV mass index showed a 25%

reduction. The patient was advised to continue with the

medications.


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6. Beta blockers reduce BP by:

a) Reducing the heart rate

b) Reduction in renin release

c) Reducing peripheral resistance

d) All of the above.

Answer is d) All of the above

Since catecholamines have positive inotropic and chronotropic

effects on the heart, beta blockers slow the heart rate, and

decrease myocardial contractility. When sympathetic activation

is low, these drugs have modest effects. However, when

sympathetic activation is high, such as during exercise and

stress, beta blockers attenuate the expected increase in heart

rate, inhibit renin release by the kidneys and diminish cardiac

output. With long term use total peripheral resistance returns

towards normal by unclear mechanisms. Beta blockers tend to

decrease the capacity to work. Exercise performance is

impaired less by selective Beta 1 blockers. Beta blockers have

important effects on cardiac rhythm and automaticity. They

reduce the sinus rate; decrease the rate of depolarization of

ectopic pacemakers, and slow conduction in the atria and AV

node. Chronic prophylactic therapy with a beta blocker in

patient's, who have had an MI, appears to help prevent the

recurrence of a second fatal myocardial infarct.


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7. What is the rationale for combining Beta blocker with

Hydrochlorothiazide?

+ Thiazide diuretics inhibit Na and Cl transport in the corticalthick ascending limb and early distal tubule, thereby reducing

blood volume; arterial stiffness and hence blood pressure. Beta

blockers reduce blood pressure by their direct inhibition of beta

receptors on the heart and reduction in renin production.

Thiazide can cause an increase in plasma renin activity which is

counteracted by beta blockers, while the cardiac dilatation

effect of beta blockers is compensated by blood volume

reduction effect of thiazides.

Over a period of time, beta blockers reduce the peripheral

vascular resistance which is further augmented by reduced

arterial stiffness caused by thiazides. Beta blockers prevent

cardiac remodeling action thereby reducing morbidity and

mortality.


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8. What are the advantages of cardioselective over non

selective Beta blockers?

Compared to non selective drugs, Bisoprolol (cardioselective)

has the following properties:

High beta1-selectivity thus less effects on the bronchus.

Lack of negative effects on carbohydrate metabolism and

insulin sensitivity. Chronic administration of Beta-blockers

may increase triglyceride levels and decrease HDL-C.Increasing cardio selectivity and increasing ISA are

associated with a more neutral effect on lipids. Bisoprolol

has been found to produce much less effect on lipids.

Increased myocardial perfusion thereby rendering a

cardioprotective effect.

Bisoprolol has a long half life and can be given as single daily

dose; thereby improving compliance. It is ampiphilic and

hence enjoys the advantages of both intermediate lipophilic

beta blockers (i.e. high absorption rate) and of hydrophilic

blockers (i.e. long plasma elimination half life) properties.

Cardioselective beta blockers are currently designated to be

first choice drugs in hypertensive patients with co-existing

medical conditions (e.g. angina, migraine, anxiety, tachycardia,

familial tremor, MI).


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9. What are the various life style measures

recommended by the JNC 7 and what is its

effectiveness?

According to JNC 7 guidelines all patients with pre hypertension

or hypertension should attempt to modify their lifestyle. This

approach is summarized below:

RModification Recommendation Approximate SBP Reduction

Weight reduction Maintain normal body weight 520 mmHg/10 kg weight loss

Adoption of DASH plan Consume a low-fat diet rich infruits and vegetables 814 mmHg

Dietary Na+ reduction


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10. What is the role of Beta blockers in Ischemic heart

disease?

Beta blockers are considered as initial therapy for chronic stable

angina, secondary prevention post-MI, and for the reduction of

morbidity and mortality in hypertensive patients. They cause

cardiac slowing and decreased myocardial contractility and may

lower arterial pressure. These effects serve to reduce the

myocardial oxygen demand especially during exercise. Beta

blockers provide symptomatic relief from angina, and improve

survival in patients with recent or prior MI. Studies have shown

that beta blockers reduce mortality by about 40 percent in

patients with ST segment elevation (Q wave) or non-ST

elevation (non-Q wave) MI.


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Close Encounter - Hypertension & IHD