Continuous wave tracing taken from the apical five chamber view illustrating the measurement of pressure half time (P1/2t) in aortic regurgitation. Here the Vmax (maximum velocity) is 479 cm/s and the slope of the Doppler tracing is 310 cm/s. Pressure half time is calculated from the slope using an algorithm by the computer of the echocardiograph. Here the pressure half time 453 msec. Pressure half time below 250 msec would suggest severe aortic regurgitation. Systemic vascular resistance, and aortic and left ventricular compliance can also influence the pressure half time, other than the severity of aortic regurgitation.

Gross cardiomegaly on Chest X-ray PA view, with gross right atrial enlargement evidenced by the shift of the right border very much into the right hemithorax. Main pulmonary artery and right pulmonary artery shadows are also prominent. Clinically and echocardiographically there was severe mitral and tricuspid regurgiation and pulmonary hypertension. Though similar enlargement of the cardiac silhouette could be noted in a large pericardial effusion, the bulges along the contour are not seen in massive pericardial effusion.  Elevated left bronchial shadow and a filling of the appendage region on the left border indicate associated left atrial enlargement.

The upper image shows the 2-D echocardiorgam in parasternal long axis view used for guiding the M-mode cut. The cursor is seen to cut the left ventricle at the chordal level, just beyond the tip of the mitral leaflets. The motion of the interventricular septum (IVS) is almost flat, due to the infarction. RV: right ventricle; LV: left ventricle; LVPW: left ventricular posterior wall

Colour Doppler echocardiorgam in AWMI

Initial view is the parasternal long axis which shows the right ventricle above and left ventricle below, with the interventricular septum in between. The aorta and left atrium are seen to the right of image. It can be seen that the mitral and aortic leaflets are opening and closing well. There is mild thickening of the anterior mitral leaflet, but there is no doming. The contractile movements of the septum is diminished. The next view is the parasternal short axis view of the left ventricle. Contractions of the anterior wall are diminished, while the inferior, posterior and lateral walls contract well. Mitral leaflets are seen in cross section in the initial view at the level of the mitral valve while papillary muscles are seen in the distal cut. Next view is the apical four chamer view which shows all the four cardiac chambers as well as the mitral and tricuspid valves. Papillary muscle and chordae attached to the anterior mitral leaflet are also seen. The defective septal motion is evident in this view. Echo drop outs in the interatrial septum can occur in this view as the ultrasound beam is parallel to interatrial septum in this view. Pulmonary veins are seen outside the left atrium, in the right lower quadrant of the image. Apical four chamber view colour flow mapping shows the forward mitral flow in red colour. There is no mitral regurgitation. The last image is the colour flow mapping in the apical five chamber view. In the apical five chamber view, the aorta is also seen in addition to the four cardiac chambers. The opening and closing motions of the aortic valve are seen in this view. The bluish colour of the flow mapping in the aorta indicates flow away from the transducer. There is some variance in the colour due to slightly higher velocity of ejection producing some turbulence in the aorta.

Blood tests

Full blood count to exclude anaemia and leucocytosis as an indicator of infection, urea and electrolytes, fasting glucose and a fasting lipid profile are the usual blood tests considered.

ECG

For patients with intermittent chest pain, ECG is often normal between episodes of pain. Look for changes suggesting coronary artery disease like abnormal Q waves, ST elevation or depression, and abnormal T waves, arrhythmias and evidence of left ventricular hypertrophy. An ECG during paing a repeat ECG after 24 to 48 hours are important add ons, often yielding valuable information. 5 – 10% of myocardial infarctions may be missed in an initial ECG. 24 hour Holter (ambulatory) ECG recording is useful in assessing the total ischemic burden, both silent and manifest.

Chest X-ray to assess cardiac size or exclude  pneumonia or pneumothorax. Coronary angiography, radionuclide imaging and cardiac magnetic resonance imaging are the other imaging modalities useful in selected cases.

Coronary angiography

Coronary angiography is of course currently the gold standard for the diagnosis of coronary artery disease, though it may miss out abluminally growing plaques, being a luminogram. Coronary angiography is undertaken for the assessment of angina uncontrolled by medication, mainly to know the suitability for coronary intervention. Angiography is also needed in case of recurrence of angina following coronary angioplasty or bypass grafting. A strongly positive exercise test is an important indication for coronary angiography. Severity of coronary narrowing is described using percentage stenosis. Thoug >50% is usually regarded as significant disease, interventions are considered only for stenosis of 70% or more.

Management of angina

There are two main therapeutic goals: Relief of symptoms and improvement of prognosis

Beta blockers should be used as the first line therapy for the relief of symptoms. They act by reducing the myocardial oxygen demand in case of angina of increased demand. Patients who are intolerant to beta blocker can be treated with calcium channel blockers, long acting nitrates and nicorandil. These agents can also be used as add on therapy when angina is not adequately controlled with beta blockers and the option for coronary revascularisation is not available.

Beta blockers

Beta-blockers reduce the effects of the sympathetic nervous system on the cardiovascular system.
Beta-1 adrenoreceptor blockers act by their negative chronotropic and inotropic effects. They also have a negative dromotropic effect in that they delay the conduction through the AV node, which is useful in controlling the ventricular rate in atrial fibrillation, contributing to relief of angina in cases in which the fast rate in atrial fibrillation has precipitated the anginal episode. Atenolol and metoprolol are  relatively specific for beta-1 receptors or “cardioselective”.

Aspirin (acetyl salicylic acid)

Aspirin is given for all patients with coronary artery disease unless contraindicated. It is one of the most important agents for secondary prevention of myocardial infarction. It has a role in primary prevention as well.

ACE Inhibitors

ACE inhibitors are initiated early in the course of myocardial infarction unless contraindicated and titrated upwards to the maximum tolerated or target dose. ACE inhibitors can be continued indefinitely in patients with preserved left ventricular (LV) function or LV systolic function, whether or not they have heart failure symptoms, to improve the long term prognosis. They can prevent ventricular remodeling in case of large infarcts and reduce the chance for left ventricular dysfunction.

Assessment/monitoring

Assess LV function in all patients who have had a myocardial infarction, by echocardiography. Measure renal function, serum electrolytes and BP before starting an ACE inhibitor or ARB and again within 1 or 2 weeks. Serial rise in creatinine should prompt evaluation for renal artery stenosis.

Angina pectoris / myocardial infarction
Pericarditis
Aortic dissection
Pleurisy
Pneumothorax
Oesophageal spasm / oesophagitis
Musculoskeleta / Costochondritis
Bornholm disease – Devil’s grip, epidemic pleurodynia

Acute coronary syndrome (ACS)

Unstable angina

Angina at rest or lowering of threshold for angina

NSTEMI (Non ST elevation myocardial infarction)

Angina at rest
ECG changes – ST segment depression and T wave inversion
If troponin or CPK-MB is elevated, it qualifies for the diagnosis of NSTEMI

STEMI (ST elevation myocardial infarction)

Similar to NSTEMI, but with ST elevation on ECG – qualifies for thrombolytic therapy

Evaluate the nature of the symptoms, history of ischaemic heart disease – patients with prior history are more at risk of further episodes. Male gender and advancing age are non-modifiable risk factors. Traditional cardiac risk factors are history of diabetes mellitus, hyperlipidaemia, smoking, and family history of cardiovascular disease (last one is non-modifiable). Past or family history of cardiovascular disease include ischaemic heart disease, stroke or peripheral vascular disease. Lifestyle factors like obesity, lack of exercise, poor diet and stress also contribute.

Approach to ACS

Brief history should assess the critical aspects mentioned above.

In patients with suspected ACS, immediate ECG should be performed
Give the patient a 300 mg aspirin orally (unless contraindicated)
Give sublingual glyceryl trinitrate to act as a coronary artery vasodilator if systolic blood pressure is over 90 mmHg and pulse is less than 100 beats per minute
Insert an intravenous cannula
Give intravenous analgesia (morphine preferred) and repeat after 15 min as necessary
Give an intravenous antiemetic along with morphine to prevent associated nausea / vomiting
If the patient is bradycardic give atropine intravenously and further doses if needed
Thrombolysis to initiated at the earliest in STEMI, if emergent angioplasty is not feasible

Evaluation of angina

History is the key
Usually there are no physical signs
ECG  may be normal most of the time
Blood pressure and BMI have to be recorded
Look for murmurs, especially an ejection systolic murmur of aortic stenosis which can cause effort angina
Evidence of peripheral vascular disease and carotid bruits have to be sought as these would suggest more severe associated coronary artery disease and have implications in management

Types of angina

Chronic stable angina
Nocturnal angina
Unstable angina
Variant angina (Prinzmetal’s angina)
Syndrome X (Cardiac syndrome X)

Unstable Angina

Unstable angina is defined as recurrent episodes of angina on minimal effort or at rest. It may be the initial presentation of coronary artery disease or it may represent the abrupt deterioration of a previously stable angina.
Crescendo angina, preinfarction angina and intermediate chest pain syndrome are also part of the spectrum of unstable angina. Angina is provoked more easily and persists for longer than stable angina. It may fail to respond to therapy. Pain is often associated with reversible ST segment depression on the ECG. Unless vigorously treated, up to 30% of patients may progress to myocardial infarction or death within 3 months

Prinzmetal’s  / Variant Angina

Prinzmetal’s angina is caused by focal spasm of angiographically normal coronary arteries. In about two thirds of patients there is also associated atherosclerotic coronary artery obstruction. In cases where there is atherosclerotic obstruction the vasospasm occurs near the stenotic lesion. The chest pain may occur at rest or wake the patient from sleep. Variant angina may be accompanied by dyspnoea and/or palpitations

Cardiac Syndrome  X

Cardiac Syndrome  X is different from the metabolic Syndrome  X. Symptoms and signs of angina occur in spite of angiographically y normal coronary arteries. They have evidence of ischemia in the form of a positive exercise test.
Syndrome X may be due to microvascular disease and is sometimes called microvascular angina.

Accelerated idioventricular rhythm (AIVR) with regular retrograde P waves. Retrograde P waves are seen just after the QRS in L2 and L3. The P waves are not that evident in L1. The retrograde atrial activation will result in regular cannon waves in the jugular venous pulse. Even though the QRS complex is almost 120 millieconds in width, at one look it may appear to be not that wide and the AIVR can be missed.

AIVR with evident wide QRS

In this tracing the wide QRS is quite evident. The P waves are not very evident, though careful examination will reveal the slight notching of the upstroke of the T waves.

AIVR with fusion and capture beats

The fourth beat shows a P wave with reasonable PR interval and a QRS which is narrower than the initial three beats, suggesting that it is a fusion beat. The last beat is preceded by a P wave and has a narrow QRS indicating that it is a capture beat.

AWMI with VPC

Deep wide Q with ST elevation seen in V1 – V3 suggesting anterior wall myocardial infarction (AWMI). Ventricular premature complexes (VPC) are also seen in bigeminal pattern. This person with anterior wall myocardial infarction developed AIVR, VPC as well as ventricular fibrillation (VF) requiring a couple of DC shocks. AIVR is an important reperfusion arrhythmia which usually needs only observation and no active treatment. If it does produce hemodynamic problems, which is quite unlikely due to the medium rates, it can be over-ridden by accelerating the sinus node with intravenous atropine. The advantage of sinus rhythm is of course, the AV synchrony, which is useful in the setting of myocardial infarction with systolic and diastolic dysfunction. Interventricular and intraventricular synchrony will also be better with sinus rhythm. AIVR is also sometimes called slow VT (ventricular tachycardia).

Unipolar VVI Pacing: Leads aVr, aVl, aVf

The sharp vertical deflection preceding each QRS complex is the pacing spike or artefact. The ECG shows a large amplitude pacing spike indicating that the pacing mode is unipolar. In unipolar mode, the electrode at the tip of the pacing lead acts as the cathode and the pacemaker can as the anode. Cathodal pacing has better threshold than anodal pacing. That is why the lead tip is programmed as cathode. In bipolar pacing, the lead tip still acts as the cathode while a proximal ring electrode acts as the anode. In that situation, as the current circuit is completed within the ventricle itself, the spillover to the surface ECG recording electrode is small so that pacing spikes are quite small and hardly visible in some leads. Temporary pacing is always bipolar and the pacemaker is not implanted within the body and hence cannot act as an anode. Permanent pacing can be programmed in unipolar or bipolar modes. Similarly the sensing of the lead can also be programmed either unipolar or bipolar. Unipolar pacing can sometimes cause local pacing in the region of the pacemaker can. This is more likely if the active side of the can is kept in contact with the pectoral muscle. Usually the pacemaker is placed within the pocket in such a way that the active side faces the posterior aspect of the skin. This will decrease the chance of local pacing in case programming in unipolar mode is required.

Even though this ECG is from a person implanted with a VVI pacemaker, it is not possible to make out that from this ECG as all the QRS complexes are paced complexes. Demand function can be identified only when there are spontaneous QRS complexes, in which case the pacemaker will wait for the programmed interval before giving out the pacing spike once it senses a QRS complex. If the sensing is defective, the pacemaker will function as a fixed rate pacemaker ignoring spontaneous QRS complexes. That mode will be termed VOO mode. Spontaneous P waves and AV dissociation are evident on close scrutiny of the ECG, especially in aVf. Lead I shows an LBBB type pattern due to the right ventricular location of the pacing lead. Inferior leads show negative QRS complexes, indicating an activation proceeding from below upwards, suggesting the location of the lead tip in the right ventricular apex. The axis will be downward in outflow pacing. Left ventricular pacing will give a right bundle branch block pattern. Pacing of the septal aspect of the right ventricular outflow tract is being evaluated as a possible way of more physiological pacing in terms of activation sequence of the two ventricles, mimicking the natural sequence.

Unipolar VVI Pacing: LeadsV1 – V3

Unipolar VVI Pacing: LeadsV4 – V6

Though we would expect a dominant positive QRS in V5, V6 in a left bundle branch block (LBBB) pattern with right ventricular pacing, when the pacing is done from the right ventricular apex, V5 , V6 shows a predominantly negative QRS complex as the activation proceeds away from the apical region. This is evident in the tracing shown above. The rS pattern in V6 is likely to be thought of as an RBBB pattern and hence indicating left ventricular pacing. But lead I and aVl show the LBBB like pattern of right ventricular pacing and so does V1, showing a negative QRS, though of smaller amplitude in this case.

Cardiomegaly on chest X-ray (CXR) PA view in dilated cardiomyopathy. The cardiothoracic ratio is increased and there is a bulge along the left border, suggesting aneurysmal dilatation of the left ventricle. This pattern could be due to ischemic variety of dilated cardiomyopathy, sometimes called ischemic cardiomyopathy or ischemic dilated cardiomyopathy. The right border is also shifted to the right, indicating right atrial enlargement. Superior venacaval shadow is seen upwards from the right atrial contour, indicating congested superior vena cava. The shadow has also a superficial semblance to the egg on side appearance, though this is not a case of transposition of great arteries.

(Click on the image for an enlarged view)

Left branch block is manifested as wide QRS with a slurred negative QRS in V1 and a slurred positive QRS in V6. The small deflection just beyond the QRS is the P wave and the next peak is the T wave. So it is evident that there is a tachycardia, possibly sinus tachycardia with a prolonged PR interval. An alternate possibility of atrial flutter with 2:1 conduction should also be thought of as the ventricular rate is around 150/minute, the classical rate for atrial flutter with 2:1 conduction. But even a close scrutiny of multiple leads do not reveal a non conducted flutter wave mid way between two proposed P waves.

Left bundle branch block and atrial tachycardia with 4:1 AV block

(Click on the image for an enlarged view)

LBBB pattern is seen just as in the ECG above. But in this tracing there are four atrial complexes for every QRS complex. The atrial rate is in the range of atrial tachycardia, nearing the flutter range. Looking back, it is possible that the upper tracing shows 2:1 conduction and the lower tracing after treatment shows 4:1 conduction because of enhancement of AV block due to the effect of the pharmacological agent which was administered in between.

Bordachar P et al (J Am Coll Cardiol, 2010; 56:747-753) et al reviewed the current data on left ventricular (LV) endocardial stimulation for heart failure. They suggest that the implementation of LV endocardial pacing will depend on development of safe, effective and durable devices which could provide reliable pacing and methods to identify optimal sites for pacing. Long term controlled trials should document the benefits and superiority of LV endocardial pacing before it can be put to clinical practice.

A study by Spragg DD et al (J Am Coll Cardiol, 2010; 56:774-781) tried to identify optimal sites for LV endocardial pacing in ischemic cardiomyopathy. They could document that LV endocardial BiV (biventricular) pacing improved the dP/dt_max over right ventricular apical pacing in all patients. In those with pre-existing coronary venous leads, pacing at transmural sites gave similar values of dP/dt_max. Optimal endocardial sites of LV pacing were located at the extreme basal lateral wall and provided better dP/dt_max than the pre-existing CRT leads. These optimal pacing sites were remote from the sites of myocardial scars at an average distance of about 9 cm.