Systemic Disorders and their Clinical Implications

Cardiovascular disease is quite common, though more frequent and severe in later life, can also affect young individuals. It is one of the leading causes of death in the world. A thorough knowledge of cardiovascular diseases is necessary because of its implications in dentistry and also the initial measures taken by the dentists in case of certain emergency conditions can be lifesaving.

Cardiovascular history taking

Clinicians must assess the status of cardiovascular system within the context of the patient’s overall health. These associated conditions can heighten cardiovascular risk during dental care. Consequently, an initial medical history should be obtained from all patients and it must be reviewed with the patient at each appointment to identify serious cardiac conditions. The clinicians should also note history of cerebrovascular disease, renal dysfunction, chronic pulmonary disease, diabetes mellitus, anemia, dyslipidemia, peripheral vascular disease, orthostatic intolerance and anemia. Further an accurate record of current medication taken by the patient, use of tobacco products, alcohol and over-the-counter and recreational drugs should be documented.

Symptoms Suggestive of Cardiovascular Disease

Common Cardiovascular Disorders and Their Dental Considerations

Hypertension

Hypertension is a disorder characterized by an abnormal elevation of arterial pressure, which if sustained and untreated, is associated with a significant increase in morbidity and mortality. The systolic or diastolic pressure or both are elevated in hypertension.

It may be asymptomatic for long periods but ultimately leads to damage with resultant symptoms in several organs including kidney, heart, brain and eyes.

It is generally accepted that a sustained systolic blood pressure of 140 mmHg or more and a sustained diastolic blood pressure of 90 mmHg or more is abnormal.

Etiology

Majority of the patients with hypertension have no cause for their disease. These patients are diagnosed to have primary, idiopathic or essential hypertension. Essential hypertension is seen in elderly, obese and individuals who are tensed and fearful. Genetic factors also play a role. However, a few patients have underlying systemic diseases that produce hypertension, which is known as a secondary hypertension.

Systemic diseases causing secondary hypertension

Renal disease (renal parenchymal disease, renal artery stenosis)

Adrenal abnormalities (primary aldosteronism,Cushing’s syndrome, pheochromocytoma)

Coarctation of aorta

Hyperthyroidism

Pregnancy (eclampsia)

Central nervous system (CNS) disorders (head injury,infection, hemorrhage and brain tumors)

Autonomic hyperactivity

Sleep apnea

Drug-induced (cyclo-oxygenase [COX-1 and COX-2] inhibitors, sympathomimetics, steroid hormones, cyclosporine and tacrolimus).

Lifestyle risk factors increasing the chances of a person becoming hypertensive are:

Obesity

High dietary salt intake

Signs and symptoms

A patient with hypertension is usually asymptomatic for quite a few years. The early symptoms include occipital headache, vision changes, ringing ears, dizziness, weakness and nose bleeding. Odontalgia due to hyperemia or congestion of dental pulp has also been reported.

Untreated hypertension reduces the life span by 10–20 years. Even mild hypertension that has not been treated for 7–10 years increases the risk of complications. Sustained hypertension results in arterial damage (atherosclerosis) and the onset of these vascular changes in the kidney, cardiovascular system, cerebrovascular system and eyes can cause complications such as renal failure, coronary insufficiency, myocardial infarction, congestive cardiac failure, cerebrovascular accident (stroke) and blindness in patients. Malignant hypertension develops in 1% of hypertensives. The chief complication is severe ischemic damage to kidney and renal failure. In the absence of treatment, it can be fatal within 1 year of diagnosis.

Blood pressure is measured by the use of a sphygmomanometer, an instrument that indirectly records the diastolic and systolic pressure.

Food, exercise, alcohol and smoking should be avoided for 30 minutes before measurement of BP and also the patient should be at rest for at least 5 minutes.

Faulty BP readings involve using improper size cuffs or applying the cuffs too loosely or too tightly.

Classification of blood pressure

Classification	Systolic BP (mmHg)	Diastolic BP (mmHg)
Normal	<120	<80
Pre-hypertension	120–139	80–90
Stage 1 hypertension	140–159	90–99
Stage 2 hypertension	>160	>100

Malignant hypertension

It is a highly elevated blood pressure associated with organ damage (eyes, brain, lungs and kidneys are affected). The systolic and diastolic blood pressures are usually more than 240 mmHg and 120 mmHg respectively.

White coat hypertension

It is a phenomenon in which patients exhibit elevated blood pressure in a clinical setting but not when recorded by themselves at home or when ambulatory. White coat hypertension is believed to be secondary to anxiety, some individuals may experience during their visit to a hospital.

General management

Acute emotions should be avoided.

In patients with secondary hypertension, manage the primary cause.

Patient should practice the following for a lifetime:

– Weight loss—maintaining ideal bodyweight lowers systolic BP reading by 5–20 points.

– Reduction in salt intake less than 2.4 g/day

– Restricting alcohol and caffeine

– Stop smoking

– Exercise (lowers BP by 5–9 mmHg)

– Intake of fruits, vegetables and low fat dairy products.

Specific management

Antihypertensive therapy

Direct-acting vasodilators: Nitroglycerin and minoxidil directly relax vascular smooth muscle. Methyldopa and clonidine act in the CNS to decrease sympathetic nervous system output.

Angiotensin II receptor blockers: Losartan and telmisartan prevent angiotensin II from binding on smooth muscle sites in arteries, promoting vasodilatation.

Diuretics: Frusemide and hydrochlorothiazide reduce blood volume and decrease vascular resistance.

Beta blockers: Propranolol and sotolol reduce heart rate, and force of contraction. Selective beta blockers are preferred. Non-selective beta blockers are contra-indicated in patients with asthma, because their beta agonist action is blocked.

ACE inhibitors: Captopril, ralopril retard renin-angiotensin system leading to vasodialatation.

Calcium channel blockers: Amlodipine, nifedipine, decrease the calcium influx in smooth and cardiac muscles, reduce total peripheral resistance and decrease force of contraction.

Alpha blocking agent: Prazosin, terazosin prevent norepinephrine from binding to receptors in arterioles leading to vasodialatation.

Therapeutic goals and pharmacologic strategies for hypertension

Therapeutic goal	Pharmacologic strategies
Reduce volume overload	Diuretics
Block beta-1 adrenergic receptors	Beta-1 adrenergic receptor antagonists
	ACE inhibitors
Dilate blood vessels	Angiotensin II receptor antagonists
Reduce sympathetic outflow from the central nervous system	Calcium channel blocking agents
	Alpha-1 adrenergic receptor antagonists
	Alpha-2 adrenergic receptor antagonists

Oral side effects of antihypertensive medicines

Drugs	Side effects
Diuretics	Dry mouth, lichenoid reactions
Beta blockers	Dry mouth, lichenoid reactions, taste change
ACE inhibitors	Loss of taste, dry mouth, ulcerations, angioedema
Calcium channel blockers	Gingival enlargement, dry mouth, altered taste
Alpha blockers	Dry mouth
Direct-acting vasodilators	Facial flushing possible, increased risk of gingival bleeding and infection
Central-acting agents	Dry mouth, taste changes, parotid pain
Angiotensin II antagonists	Dry mouth, angioedema, sinusitis, taste loss

Dental considerations

Patients with controlled hypertension can receive dental care in short appointments.

Anxiety and pain should be avoided since endogenous epinephrine release in response to pain or fear may induce dysrhythmias.

Preoperative reassurance and sedation with 10 mg temazepam or 5 mg diazepam may be helpful.

Raising patients from supine position may cause postural hypertension and loss of consciousness if patient is using thiazides, calcium channel blockers.

Aspirating syringe should be used to give local anesthesia to avoid intravenous entry of epinephrine.

Epinephrine in local anesthesia is not contraindicated unless systolic pressure is over 200 mmHg or diastolic pressure is over 115 mmHg.

Epinephrine containing local anesthesia should not be given in large doses in patients taking non-selective beta blockers since interaction may induce hypertension and cardiovascular complications.

Gingival retraction cords containing epinephrine should be avoided.

Administration of two to three cartridges of local anesthesia with epinephrine 1:100,000 will not cause cardiovascular changes.

Epinephrine should be used with caution in patients taking tricyclic antidepressants and diuretics since acute hypertensive changes and dysrhythmias, respectively may occur.

Ischemic or Coronary Heart Disease

It is one of the most common medical problem in general population. Coronary heart disease is an inflammatory disease affecting the large and medium sized arteries of heart resulting in inadequate or decreased coronary blood flow. Atherosclerosis and hypertension are the major contributory factors.

Atherosclerosis basically refers to the formation of fibro-fatty lesions in the walls of arteries. These may increase in size to cause stenosis of the vessels reducing the blood flow to the heart on exercise. This is known as angina. In the later stages, the atherosclerotic plaque ruptures and exposes the arterial blood to the plaque contents and stimulates the formation of hemostatic plug. This occlusive thrombus may cause myocardial infarction.

Risk factors

Non-modifiable factors

1. Family history: Presence in patient’s parents, increases the risk of occurrence in patients at an early age.

2. Gender: Men between 25 and 65 years of age are more prone and women at post-menopausal age.

Modifiable factors

1. Total cholesterol of more than 240 mg/dl is associated with ischemic heart disease.

Elevated LDL, decreased HDL, increased total to HDL cholesterol and hypertriglyceridemia also contribute. Statins and fibrates correct lipid abnormalities.

2. Hypertension: Systolic pressure more than 140 mmHg or diastolic pressure more than 90 mmHg increases the chances of ischemic heart disease.

3. Smoking: Women who smoke more than 19 cigarettes per day are likely to have ischemic heart disease.

4. Other risk factors are diabetes mellitus, obesity, lack of exercise, lack of fruits and vegetables in the diet, alcohol use, stress, elevated levels of C-reactive proteins.

Angina Pectoris

It is the most common clinical presentation of ischemic heart disease and is infrequent before the age of 40 years. It may be defined as a temporary inability of the coronary arteries to supply the myocardium with the sufficient amount of circulated blood. Atherosclerotic narrowing of the coronary arteries is an important cause of this imbalance in oxygen supply. It is rarely caused by spasm of the blood vessels. Initially, the atherosclerosis does not lead to any symptoms. However, the obstruction becomes large over a period of decades to cause pain. The pain of angina is described as a sense of choking, tightness, heaviness, or compression of the chest, sometimes radiating to the left arm or jaws. The common precipitating causes include physical exertion and emotions.

Levine’s sign is characteristic of ischemic chest pain. It is seen in angina pectoris and myocardial infarction. This sign described by Dr Sam Levine who observed many of his patients suffering from chest pain hold their fist over the chest.

Variants of angina

Stable angina

Pain only on exertion and relieved by rest within 10 minutes. Stable angina is caused by fixed atheromatous plaque in one or more coronary arteries.

Unstable angina

Angina at rest, angina appearing more frequently, appearing at lower level of exertion, requiring larger doses for relief or relief taking longer. It is caused by dynamic obstruction of coronary artery due to plaque rupture with superimposed thrombosis and spasms.

Prinzmetal’s angina

Angina at rest and occurs commonly at night caused by coronary artery spasm.

Management

Pain is relieved by nitroglycerin. Nitroglycerin lowers peripheral vascular resistance and lowers oxygen demand of the heart.

Drugs such as aspirin are used to inhibit platelet function.

Beta adrenergic blockers prevent the effects of cardiac sympathetic stimulation and reduce myocardial oxygen demand by decreasing the heart rate, ventricular systolic pressure and peripheral arterial pressure.

Calcium channel blockers prevent calcium from entering muscle cells (arterial or cardiac muscles) thus preventing contraction leading to vasodilatation.

When angina does not respond to drugs, coronary angioplasty, percutaneous coronary arterioventral procedures or bypass grafts are indicated.

Dental considerations

Preoperative nitroglycerin can be given prophylactically before dental therapy.

Effective local anesthesia is a must. Long-acting local anesthesia with bupivacaine can be used with vasoconstrictor to prolong the effect of local anesthesia. Aspirating syringe is a must.

Increased heart rate and blood pressure during long appointments indicate need to conclude dental care.

If a person develops angina during dental treatment, the procedure should be terminated and the patient should be seated in semi-inclined position and the patient should be given nitroglycerin 0.3–0.6 mg sublingually. If pain persists even after 3 minutes, additional doses (up to 3 mg) every 5 minutes should be given and medical help should be sought. If pain persists, 300 mg of chewable aspirin is given. Moreover, morphine sulfate (IV) relieves pain and anxiety.

Nausea, bradycardia, hypertension indicating myocardial infarction may occur.

Tricyclic antidepressants are contraindicated. Conscious sedation and general anesthesia should be deferred for 3 months in patients with recent onset angina or unstable angina.

Myocardial Infarction

It is a severe form of coronary artery disease. An anginal pain lasting longer than 30 minutes is considered to be a myocardial infarction. The pain may be accompanied by nausea and vomiting, tachycardia, grossly irregular pulse, pallor and difficulty in breathing, sweating, and restlessness. About 10% have painless infarctions.

Diagnosis

The diagnosis of acute myocardial infarction is based on the presence of two of the following three criteria: (1) signs and symptoms compatible with myocardial ischemia, (2) typical ECG changes—ST segment elevation at the end of the PR segment, (3) measurement of creatinine kinase (CK) and myocardial-bound CK (CK-MB).

Elevations in the serum troponin T and troponin 1 levels, which are sensitive markers for myocardial injury, have also been used to test for acute myocardial infarction.

Therapeutic goals and pharmacologic strategies for coronary heart disease

Therapeutic goals	Pharmacological strategies
Inhibit progression of atherosclerosis	Lipid-lowering agents HMG-Co-A reductase inhibitors
Improve circulation in coronary arteries	Nitrated calcium channel blockers
Reduce workload	Beta-1 adrenergic receptor antagonists
Prevent thrombus formation	Antithrombotic agents
Prevent coagulation	Anticoagulants

Dental aspects

1. Physician’s consent is necessary before treating the patient.

2. Patients within 6 months of an MI (recent MI) are at the risk of further complications, hence, elective dental care should be deferred. However, the first 6 weeks is more critical, and with the physician’s consent, simple emergency dental treatment under LA may be done during the first 6 months.

3. Anxious patients may be given preoperative glyceryl nitrate.

4. Effective local anesthesia is important.

5. Aspirating syringes must be used.

6. Use of epinephrine impregnated gingival retraction cords should be avoided.

Management of myocardial infarction

Same as that of angina.

Additionally, patients are on platelet inhibitors. Care should be taken to prevent significant bleeding.

Local hemostasis should be promoted (procoagulant materials such as collagen or topical thrombin should be used). Local pressure should be applied for a longer duration. Injecting vasoconstrictor containing local anesthesia directly into surgical site and using sutures is not required.

Congenital Heart Disease

It is a common heart disease among children, present in 1% of live births. Congenital defects involving heart or adjacent vessels may be associated with other congenital anomalies. These congenital anomalies can be cyanotic or acyanotic in nature.

Cyanotic

Transposition of great vessels, tetralogy of Fallot, Eisenmenger’s syndrome. Cyanotic defects are lethal.

Acyanotic

Atrial and ventricular septal defects, patent ductus arteriosus, coarctation of aorta, pulmonary stenosis, mitral valve prolapse, aortic stenosis.

Causes

Idiopathic

Acquired (congenital rubella, maternal drug misuse).

Clinical features

Most striking feature in some congenital heart disease is cyanosis (more than 5 g reduced hemoglobin per deciliter of blood)

Causes severely impaired development and often gross clubbing of fingers and toes

Eventually polycythemia develops

SCyanosis due to right to left shunt leading to chronic hypoxia

Shunt from left to right leads to pulmonary hypertension, direction changes later leading to cyanosis

Patients with congestive heart disease liable to infective endocarditis and others are pulmonary edema, polycythemia, bleeding tendency, growth retardation, fatigue and brain abscess.

Dental considerations

Antimicrobial prophylaxis

Bleeding tendencies due to platelet dysfunction and excessive fibrinolytic activity

Dental bacteria may cause cerebral abscess

Aspiration during local anesthetic procedure is a must due to epinephrine in local anesthesia

Gingival retraction cord containing epinephrine should be avoided.

Oral manifestations associated with congenital heart diseases

Delayed eruption of both the dentitions

Greater frequency of positional anomalies

Enamel hypoplasia

Teeth have bluish white skimmed milk appearance and gross vasodilatation in pulp

Greater incidence of caries and periodontal activity.

Rheumatic Fever

Rheumatic fever is the most common cause of cardiac valve disorders. The mitral valve is affected more frequently. It results from an altered immunologic response to a group A beta hemolytic streptococcal pharyngitis, leading to formation of Aschoffs nodules in the myocardium which develops 1–3 weeks after the streptococcal infection. Though, only 3% of cases of beta hemolytic pharyngitis resulting in rheumatic disease, there is no way to forecast which individuals will have rheumatic heart disease (RHD).

Common manifestations include new onset murmur, carditis, polyarthritis, chorea, erythema marginatum, fever and subcutaneous nodules (modified Jones criteria). The beta streptococcal infection is confirmed by increased serum antistreptolysin O (ASO) antibody titer or positive throat culture. RHD resulting in valvular injury is confirmed by echocardiography for any patient with a history of rheumatic fever, it is imperative to determine whether the infection resulted in RHD.

Dental considerations

Consult with the physician

All rheumatic heart lesions are at the risk of infective endocarditis and hence precautions and treatment similar to infective endocarditis should be carried out

Local anesthesia can be given

General anesthesia should be avoided.

Infective (Bacterial) Endocarditis

Infective endocarditis (IE) is a rare, potentially lethal infection, predominantly affecting heart valves. The endocardium can also be affected. It results from bacteremia originating from any site and representing almost any species. It is caused mainly by bacteria as well as fungi.

Bacterial endocarditis can be defined as an infection that affects the endocardium in valvular, mural and septal defects, as well as in arteriovenous and arterioarterial shortcircuits.

It usually occurs in older individuals, peak prevalence is 6th or 7th decade. It is less frequent in the young, except in intravenous drug users. It occurs predominantly in males. Most patients have pre-existing cardiac disease. The mitral valve is more frequently affected followed by aortic valve and tricuspid valve. Sterile vegetations, i.e. comprising of platelets and fibrins accumulate over the damaged valves and these get readily infected during bacteremias resulting in infective endocarditis.

Main groups affected by infective endocarditis	Approximate percentage of all cases of infective endocarditis
No obvious cardiac valve disease	40%
Chronic rheumatic heart disease	30%
Congenital heart disease	10%
Prosthetic cardiac valves	10%
Intravenous drug abuse	10%