Main Message

 

Þ    Main burden of cardiovascular diseases comprises of hypertension and Ischaemic Heart Disease.Hypertension is a silent killer. Many patients of I H D are also silent paricularly in diabetics and elderly females. So it is the duty of physician to remain alive to the possibilities of these silent phenomena. It is the doctors who have to diagnose these. All it takes is, to screen their patients from time to time for hypertension. Their suspicion for I H D should be enhanced in high risk patients.

 

Þ    Discontinuation of antihypertensive therapy by the patients is partially the fault of treating physician. It is his job (whatever it takes) to convince the patient that he must continue it for life. Pass the relevant information on nature of disease to the patients again and again. If patient waits for symptoms then he is inviting lot of trouble. Therapy is most beneficial before the symptoms appear. This is the message for patients. Headache is not a specific symptom of hypertension.

 

Þ    Angina is the diagnosis based upon only and only history. No investigation is involved. This should be clearly understood and practiced as such. Learn the typical, atypical and rare presentations of angina. Other presentations of I H D are also mainly based upon history but here these can be confirmed with investigations. Silent AMI must remain on the list of D/D of physicians in patients presenting with unexplained acute heart failure,profused sweating and normalization of BP in a previously hypertensive patients.

 

Þ    Valvular heart disease should be picked upon physical examination. It should not be missed. It should be confirmed by echocardiography.

 

Þ    Family physicians must have a working knowledge of cardiovascular medicine. Pathogenesis of diseases should be clear in the minds. Drugs, their mechanism of action, interaction with other drugs and therapeutic indications should be well understood. All these aspects of therapeutics are rapidly changing.

 

Þ    Hypertension and I H D is appearing more and more at younger age groups. There were times when these were considered as part of aging process. The word Essential in ESSENTIAL HYPERTENSION denoted that with aging blood vessels get harder and harder. So increase in blood pressure is essential. But this concept is no more accepted. Practical Implication = Include younger patients in screening when necessary.

 

Þ    High systolic blood pressure is more dangerous than rise in diastolic blood pressure particularly in elderly patients. This is also contrary to what used to be believed few years ago.

 

Anatomical and Physiological Considerations.

 

Left ventricle is mainly supplied by left coronary artery. Right Coronary Artery also contibutes to some extent in the blood supply of left ventricle. Right ventricle is exclusively supplied by right coronary artery. Atria are thin walled as compared to ventricles. Basic function of chambers is to store and pump blood. Whenever there is disproportionate increase in volume of blood handled by any specific chamber there is an appropriate response. Atria respond by increasing the size i.e dilatation. Ventricles first increase the force of contraction in response to increased pressure such as in Aortic Stenosis, or increased volume such as in Aortic Regurgitation (Frank Starling Law). Ventricular muscles hypertrophy in response to pressure and maintain the force required for ejecting.This is concentric hypertrophy. Xray chest does not show it. When this hypertrophy fails to cope with increased load then fibroblasts start replacing myocites. Fibrous tissue increases and heart starts to dilate.In volume overloaded condition heart size increases from the onset.

 

Endothelium:  Just few years’ back this tissue was considered as inert tissue. But now it is known that it is very active tissue and it can be taken as an organ. This produces hormones and enzymes. Turnover of these substances is quite dynamic. Renin Angiotensin System is also part of its activity.

 

 

Hypertension

 

v     It is a life long disease. So do not label patient in haste or in one visit unless BP is very high or there are strong risk factors with family history or there is evidence that target organs are affacted. Otherwise delay in initiating the treatment for few weeks will not make much difference.

v     There are wide variations in blood pressure over 24 hours. Walking, anxiety and even a visit to a doctor can increase blood pressure. So when patient is examined, please make sure he has properly rested after walking in to your clinic. Then take the history and do the examination. Blood pressure may be taken at the end of examination when anxiety level is minimum. Monitor for diunal variations for two months. If BP remains high then therapy can be instituted and patient must be educated that this therapy is life long with time to time adjustment in the doses and drugs.

v     Can antihypertensive therapy be discontinued? If blood pressure remains normal with therapy for 3 years and there is no target organs involvement, this may be contemplated. Gradually withdraw drugs. If after total withdrawal of drugs BP remains normal for one year (there is no rebound increase in BP) it may be assumed that hypertension has been cured.

v     Blood pressure should be taken in both supine and sitting position. There is usually  a difference of 20 mms in both readings.If there is a rise in BP on sitting it may suggest high renin state,where ACE inhibitors will be more effective.

v     In obese patients BP reading is usually higher than in non-obese patients. Each Kg increase in weight leads to increase of 1-1.5 mms in BP.Cuff size must be appropriate in such patients.3/4^th of circumference and at least 50 % of hieght of arm must be covered by the cuff.

v     Oral contraceptives may be avoided in-patients who are receiving antihypertensive therapy. Other measures for contraception may be adopted.

v     Anxiety may lead to temporary increase in BP reading. There must be other sings of anxiety,like tachycardia, present in such patients. If it is so then BP may be monitored for 24 hours with Holter or patient may be examined repeatedly for 2 months. Anxiety in itself does not lead to hypertension. Sedatives have no role, whatsoever, in the treatment of hypertension.

v     Low Renin Patients:        If BP is highest when patient is supine i.e lying flat, this suggests low renin hypertension. These are the patients where is there is volume overload. Intravascular volume is increased. When patient lies down, venous return from lower extremities improves. This increases the cardiac output leading to increase in blood pressure when patient is in supine position. When this patient will assume sitting position, fluid will accumulate in lower extremities leading to decrease in cardiac output and blood pressure. Difference is usually >20 mms. Diuretics are best as first step for these patients.

v     High Renin Patients:       These are the patients where BP is usually higher in sitting position rather than in supine position. Decrease in intravascular volume prompts an increase in renin. For these patients ACE inhibitors are the prefered therapy.

v     Base line Investigations in all hypertensives before starting therapy should be ordered. Urine, XR Chest, CBC (to monitor the drug effects on haemopoeitic system), ECG, Blood glucose level, renal profile,serum uric acid and Na + & K+ levels are routine investigations. Catecholamines levels can be ordered if considered necessary. Sodium and Potassium levels are done to rule out HYPERALDOSTERONISM.Catecholamine levels, which are now done in Lahore by good laboratories, can replace URINARY VMA. This is needed only when other features of Pheochromocytoma are present.

v     Single agent may be used for mild to moderate hypertension. Concomitant presence of anxiety in hypertensive patients suggests use of betablockers. In diabetics ACE inhibitors may be drugs of first choice. Diuretics should be avoided in diruetics,hyperlipidaemic and hyperurecimic patients. Indepamide is also a mild diuretic. It is also a mild vasodilator.

v     Combination of different drugs is valid if these have synergistic effects. Calcium Channel Blockers (CCB) may be combined with diuretics. ACE inhibitors can be combined with betablockers. In elderly patiets where SA & AV nodes dysfunction may be present CCB in combination with Beta Blockers may be avoided due to negative chronotropic properties of both agents.

v     Oedema produced by CCB may be left alone after explanation to the patients that it is not harmful.

v     Spironolactone is beneficial in heart failure patients. It has antifibroblastic activity. It reduces or retards fibrosis in myocardium.

v     In young patients betablockers and diuretics may be avoided. Calcium channel blockers and ACE inhibitors are drugs of choiche in younger age groups.

v     Kidneys excrete Betablockers. So these should be avoided in renal failure. Only one betablocker, metoprolol, is excreted by liver. This may be a used in patients of renal failure.

v     Pregnancy Induced Hypertension is an intravascular volume depletion condition. So diuretics are contraindicated. Peripheral vascular resistance is also high in pregnancy induced hypertension. It reduces cardiac output. ACE inhibitors are totally contraindicated due to adverse effects on foetus. Aldomet is time-tested drug. This is least harmful. Nifedepine can be used. Low dose aspirin should accompany all anithypertensive therapy. Bed rest may become essential if BP is not controlled.

v     Calcium Channel Blockers.There are further three subgroups in this large group.

(Inotropic = Increase in heart force.Chronotropic = increase in heart rate)

1                    Dihydropyridine like Nifedepine.This group dilates arteries and veins in periphery.This has positive chronotropic effects.Reflux tachycardia is due to vasodilation.Amlodipine is also in this group.

2                    Derivatives of Benzodiazepines like Diltiazem.It is a mild vasodilator.It has negative inotropic effect.

3                    Papaverine Derivative.Verapamil.It has most marked negative inotropica as well as chronotropic effect.

 

 

Ischaemic Heart Disease

 

This is the second most common disease in CVS in our clinics. Younger age groups are being affacted now.Patients in their thirties are suffering IHD.Two peculiar points may be noted.

 

1.      Diagnosis is almost always based upon history in those presenting with Angina.

2.      AMI may be silent.You must be aware of at least atypical features of M.I.

 

Nerve Supply and Ischaemic Pain

 

Myocardium has no pain nerve fibres.Heart is supplied by the autonomic nervous system. Parasympathetic fibres from vagus nerve and sympathetic nervous supply are through cervical ganglion from last cervical and first two dorsal segments of spinal cord. These sympathetic fibres reach heart along the coronary arteries from the sympathetic ganglion. These fibres travel in spinal cord in anterolateral columns, which are adjacent to spinthalamic tract, which carries impulses regarding temperature, touch and pain. It is postulated that somewhere along the travel path there is some intermingling of fibres of sympathetic column and spinothalamic tract. Ischaemic pain may contain sensations of these three varieties and is felt in the distribution of the these spinal segments from C5 to T 2 of brachial plexus. Via the nucleus of Trigeminal nerve which streches to upper segments of spinal cord,pain may be refered to face and lower jaw.

So Ischaemic pain may be refered anywhere from umblicus upwards to the neck, jaws, both arms, and back of the chest. This may also contain elements of touch (e.g numbness), temperature i.e burning, and different types of pain.

 

Angina

 

This is a diagnosis based upon nothing but history. Still it is being missed more than expectations. No investigations are required to confirm the diagnosis,if the presentation is typical. Clinical presentations fall into three categories.

 

1  Typical = 50-60 %                         2 Atypical = 40-50 %             3 Rare

 

This means in almost half of the patients,presentation will be atypical. This is a large percentage. Atypical presentations are as important as typical ones.

 

Typical presentations

 

The patient may describe pain or discomfort or sensations by many different words. These may be

Pain or burning

·        Shortness of breath

·        Feeling of Heavyness

·        Feeling of discomfort

·        Feeling of Choking

·        Numbness

·        Constrictive feelings

·        Different cultures and classes use different words.

Constant features of Typical Presentations

 

v     Area: From umblicus to chest.This may be radiated to neck to jaws, back of chest, shoulders and both arms.

v     Onset with exertion

v     Relief on rest.

v     Duration is in few minutes.

 

Associated Features.

 

Anxiety                       Perspiration               Sense of impending disaster

Timings

 

·        Early Morning Angina These complaints may be more or only in the morning.

·        More frequent in extremes of weather.

·        May appear 15-20 minutes after meals.

·        Walk Through Angina:    Patient may be able to continue the activity despite the symptom, in the morning, and symptom may disappear after few minutes. Then this may not reappear during whole of the day.

 

These are as important as typical features. These are being missed more than typical ones. So these need more stress. In the above mentioned area any complaint of upper GIT or general nature which is brought on with exertion or after meals, lasting only for few minutes, occuring repeatedly under same circumstances need to include angina in the list of differential diagnosis.These fall into many varieties.

 

Symptoms related with G I T.

 

Due to Vagal Nerve.These are more common in-patients in which diaphragmatic surface of heart is involved. This is supplied by right coronary artery. Symptoms appear after heavy meals or exertion after meals. Patient may describe his feelings in following words.

 

v     He feels unpleasant fullness after meals.

v     Burning or Gas in epigatrium and retrosternal area

v     He may experience eructations.

v     Or he may have all symptoms described above as typical symptoms after meals.

v     Any Upper G I T symptom which appears after meals, especially if exertion precipitates it, angina should be in the list of differential diagnosis.

 

Other Symptoms

 

v     Recent onset of shortness of breath after mild exertion, in the absence of other underlying diseases like valvular heart disease or hypertension.

v     Weakness, listlessness

v     Sweating with exertion or after heavy meals.

 

v     Atypical symptoms are more common in-patients above 60 years of age. In young female patients shortness of breath, sweating and other sympthetic nervous system symptoms do not carry the same importance.

 

Risk Factors & Atypical Symptoms.

 

All atypical symptoms make it mandatory to rule out I H D by investigations if risk factors for I H D are present in such patients. Followings are the risk factors.

 

1        Age            2 Family history         3 Hypertension           4  Smoking

5        Diabetes Mellitus                         6 Hyperlipidaemia     7   Obesity.

 

Rare Symptoms.

 

Any kind of symptom which occurs again and again on the same amount of exertion in the same area prescribed for the Symptoms of I H D needs to be investigated for I H D.One example from his practice was given.

There was a patient who felt pain in his right thumb on walking. This was always there after same amount of exertion. He has been to many physicians. ECG was normal. It was daignosed as angina on ETT when changes in ECG occurred just at the time when he described pain. Angiography revealed 90 % blockage in coronary ateries.

 

Unstable Angina

 

Whenever above mentioned typical and atypical symptoms occur at rest lasting for less than half an hour warrants a diagnosis of unstable angina. These symptoms need to be confirmed with investigations. Withen few days this condition will settle down either as angina or it will progress to AMI.Angina patients of recent onset or progressive angina or those patients who need increasing amounts of nitroglycerin to relieve pain can also be labelled as unstable angina.

 

Acute Myocardial Infarction

 

All above-mentioned symptoms when continue for more than half an hour and severtiy is very high,AMI should be suspected. Pain is usually very severe. It is not relieved with rest or nitroglycerin. Sweating, sense of impending disaster, apprehension is prominent accompaniments of pain. Shock may be present. If diaphragmatic surface of heart is involved, upper GIT symptoms like nausea and vomiting are present. ECG should confirm the diagnosis.

 

AMI may be silent. Only indications may be sweating, weakness, nasea, vomiting, hypotension, shortness of breath, giddiness, dizziness, restlessness or any other general symptom. In all those patients whose risk profile is very high appropriate investigations should be carried on to rule out AMI

 

AMI may cause sudden death. Most rapid deaths are caused by AMI with ventricular fibrilation.

 

Narrowing of Coronary Arteries

 

Normally endothelium is smooth surfaced. It is distrubed in Diabetes Mellitus, Hypertension or in smokers. First abnormality is usually a small tear in endothelium. Then through this tear material like blood cells, platelets etc,start accumulating in the place. Tear is repaired by endothelial cells. So these accumulated cells under the endothelium keep on proliferating at this site. Indigenous growth factors produced in endothelium accelerate this process. This growth and accumulation at one spot is like a slowly growing tumour. Lumen of the vessel becomes compromised. It becomes narrower and narrower. As the process is slow this may allow formation of collaterals in the area of supply.

 

There is another endpoint for this atheroma. When the fibrous tissue covering the this collection of platelets and macrophages in the endotheliam is yet not firm and it is young, it may be eaten up by an activated macrophage. Activated macrophage means that this macrophage is charged up with proteolytic enzymes as a response to inflammation at some other site in the body. In this case all the products accumulated at this spot may burst open producing a raw surface on the endothelium.This raw surface is an ideal site for thrombus formation leading to thrombus formation.

 

Precipitating factors for Ischaemic Pain

 

Narrowing of the vessels may be there but the blood supply may be enough for the area untill some extra demand is made by someother pathology. The diseased vessel may not meet this. So angina or USA or AMI can be precipitated. Following factors can exaggerate the presentation of IHD.

 

·        Anaemia

·        Hypertension

·        Thyrotoxicosis

·        Infections:Fever

·        Tachycardia

·        Irregular rythem