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48 year old male, non smoker presented with acute onset severe retrosternal chest pain for preceding 8 hours. The pain was associated with heaviness over chest and radiated to neck and was intermittent with each episode lasting for 5-10 minutes. It aggravated on exertion and was associated with profuse diaphoresis and anxiety. He also complained of palpitations of 6 hours duration which were abrupt in onset, regular and relieved spontaneously. There was history of a single episode of loss of consciousness following chest pain which lasted for about 30 seconds, with a spontaneous and complete recovery. He denied any history of dyspnoea on exertion, orthopnoea or PND. There was no history of preceding fever, cough, expectoration, hemoptysis or wheezing.
There was no history of similar episodes in the past or history of hypertension, diabetes, ischemic heart disease or any major illness. A significant family history was that younger brother suffered an acute myocardial infarction at 41 years of age and father was a documented case of coronary artery disease since 45 years of age. He consumed a mixed diet and denied any addictions.
What is the most likely diagnosis in this case?
As per the presentation of the patient with acute onset, substernal chest pain with aggravation on exertion, most likely he has anginal chest pain.
How do you differentiate typical, atypical and non anginal chest pain?
Typical anginal chest pain has three characteristics- being substernal, provoked by exertion and relieved by rest or nitroglycerine. Anginal chest pain correlates with a high risk of coronary artery disease in all age groups. If any two of these three characteristics are present, it is called an atypical anginal chest pain, which has an intermediate risk for CAD in women older than 60 years and men older than 40 years. Non anginal chest pain has any one of these three features.
What are the examples of non coronary life threatening chest pain?
Among disorders of the heart, aortic dissection and acute pericarditis are serious illnesses which may mimic angina. Spontaneous pneumothorax, pulmonary embolism, and rupture esophagus are other causes of non coronary life threatening chest pain.
How do you define significant family history of CAD?
As per the Framingham study, history of any first degree male relative < 55 years and female relative < 65 years suffering from CAD is considered to be significant family history.
Examination & investigations
On Examination, patient had a BMI of 27.11 kg/m2, he was afebrile, had a pulse of 96/ min, regular, euvolemic, bilaterally symmetrical and all peripheral pulses felt with no radio-femoral delay. He was normotensive with a BP of 112/78 mmHg and respiratory rate of 16 /min, abdomino-thoracic, maintained a saturation of 92 % at room air. JVP was not raised, and there was no pallor, cyanosis, icterus, pedal edema, clubbing or lymphadenopathy. There were no markers of dyslipidemia or insulin resistance.
On cardiovascular auscultation, S1 and S2 were heard along with LVS3. There were no murmurs or any other adventitious sounds heard. Chest auscultation revealed bilateral vesicular breath sounds and no adventitious sounds. Abdomen was soft and non tender with no palpable organomegaly or free fluid. Other systemic examination was normal.
An urgent ECG revealed T wave inversions in lead III, aVF, and V1-V4. Other investigations revealed Hemoglobin- 12.3 g/dl, total leucocyte count- 11,200/cmm and platelet count - 2.34 lac /cmm. Metabolic parameters including liver and renal function tests and random blood sugar levels were normal. A bedside qualitative Trop- T test was negative and CK-MB levels were 22 IU/L.
A bedside 2 D echo showed an ejection fraction of 40% along with septal, apical and anterior wall hypokinesia. The Right atrium and ventricle were dilated and there was moderate tricuspid regurgitation.
The patient was diagnosed as a case of acute coronary syndrome- unstable angina and was managed with oxygen inhalation by face mask, Inj LMWH (Clexane) 60mg 12 hourly, antiplatelets (Aspirin and Clopidogrel), Tab Metoprolol 25mg 12 hourly and Tab Atorvastatin 80 mg HS. With this management, patient had no recurrence of chest pain or palpitations and no further syncopal episodes, but he complained of extreme fatigue and was found to have low normal BP recordings along with tachycardia.
On taking detailed history, patient revealed that he has had recurrent deep venous thrombosis (left lower limb) in 1994 and 2000, documents of which were not available. Patient had developed hypotension (BP- 100/60 mm Hg) along with persistent tachycardia (P-110-120/min). A bedside 2 D echocardiography was repeated which showed RA/RV dilatation and septal, apical and anterior wall hypokinesia. A review of the ECG showed S1Q3T3 pattern(Fig 1).
Fig 1: ECG showing sinus tachycardia & S1Q3T3T
The patient was suspected to have pulmonary thromboembolism on the basis of history of prior DVT, tachycardia, hypotension, ECG changes and RA/RV dilatation on 2D Echo.
When should one clinically suspect Pulmonary Thromboembolism?
The classic triad of PE includes -hemoptysis, dyspnea and chest pain: which is neither sensitive nor specific. It occurs in fewer than 20% of patients. Among patients with massive PE, only 60% have dyspnea, 17% have chest pain, and 3% have haemoptysis. Many patients are initially completely asymptomatic. An atypical presentation with seizure, syncope, abdominal pain, high fever, productive cough, new onset of reactive airway disease ("adult-onset asthma") may also be seen in rarely.
Enumerate the clinical findings and their frequency in PE?
The most common symptoms of acute PE are acute or subacute onset dyspnoea, and chest pain. Small peripheral emboli can cause pulmonary infarctions and can present with pleuritic chest pain and hemoptysis. Patients may also present with cough, palpitations and fever. The most common findings on examination are tachypnoea and tachycardia. Patients with massive PE generally present with hypotension and features of shock which are markers of high risk. These patients may also have elevated JVP, left parasternal heave and loud P2, features of pulmonary hypertension, along with findings of right heart failure.
Clinical finding Frequency
Accentuated S2 53%
S 3 or S 4 gallop 34%
Clinical signs and symptoms of thrombophlebitis 32%
Lower extremity edema 24%
Cardiac murmur 23%
What are Well's Criteria for PE?
The initial assessment of the clinical probability of pulmonary embolism is based on either clinical judgment or clinical decision rules (Wells and revised Geneva scores).The assessment of pre-test probability (PTP), with categorization into low-, moderate- and high-risk groups is an essential initial step in the current diagnostic management of patients with suspected VTE. The prevalence of VTE in these categories is <10%, 20-30% and 60-80%, respectively. The PTP of VTE can be assessed empirically or by using scoring systems based on a clinical decision rule.
Alternative diagnosis less likely than PE
HR > 100 bpm
Immobilisation/ Previous Surgery
Malignancy (active within 6 months)
Traditional clinical probability assessment (Wells criteria)
Moderate 2.0 to 6.0
Simplified clinical probability assessment (Modified Wells criteria)
PE likely >4.0
PE unlikely â‰¤4.0
How do you calculate Modified Geneva score for PE?
The simplified Geneva score can also be used for calculating the pretest probability of PE in a given patient.
The simplified Geneva score
Age 65 years or over
Previous DVT or PE
General anesthesia or fracture within 1 month
Active malignant condition or malignant condition that has been cured within 1 year
Unilateral lower limb pain
Pain on deep palpation of lower limb and unilateral edema
Heart rate of: 75 to 94
Heart rate of: Greater than 94
Likelihood of patients having a PE with a simplified Geneva score less than 2 and a normal D-Dimer is approximately 3 percent. Patients with a score of 2 or less are considered unlikely to have a current PE.
Geneva score for PTE
Probability of PE (%)
What are the ECG signs of PE?
ECG abnormalities exist in many patients with PE without preexisting cardiovascular disease. In a significant number of patients these are nonspecific, thus limiting the specificity and sensitivity. The most common signs are sinus tachycardia, right axis deviation, and right bundle branch block (8 - 69% of people with PE).
Electrocardiographic findings historically considered being suggestive of PE - large S wave in lead I, large Q wave and an inverted T wave in lead III ("S1Q3T3") is infrequently seen in acute PE. However, this is common among patients with massive acute PE and cor pulmonale. In one prospective study, 70 percent of patients with acute PE had ECG abnormalities, most commonly nonspecific ST-segment and T-wave changes.
ECG abnormalities associated with a poor prognosis are:
Â â€¢ Atrial arrhythmias
Â â€¢ Inferior Q-waves
Â â€¢ Right bundle branch block
Â â€¢ Precordial T-wave inversion and ST-segment changes
ECG-based scoring systems have been developed to correlate ECG findings with the severity of embolism, but the clinical utility of these systems remains speculative.
What are the X Ray signs of PE ?
Radiographic abnormalities are common in acute PE and seen in approx 88% of patients. The most commonly seen abnormality is atelectesis (60-70%) without infarction. The 'classic' findings include-
Westermark sign- increased lucency in area of embolus.
Hampton's Hump- wedge shaped pleural based infiltrate.
Palla's sign- dilated right PA.
Abrupt cutoff of vessel
What is the role of Echocardiography in diagnosis of PE ?
Only one third of patients with submassive PE have echocardiographic abnormalities suggestive of acute PE.These include- increased right ventricular (RV) size, decreased RV function and tricuspid regurgitation. In cases of massive PE, however, these abnormalities are more likely and echocardiography may be useful if a rapid presumptive diagnosis is required to justify the use of thrombolytic therapy suggestive of PE . These include- regional wall motion abnormalities that spare the right ventricular apex also known as "McConnell's sign" (which has 77% sensitivity and 94% specificity for diagnosis) and direct visualization of a RV thrombus. However, only 4 percent of patients with PE have an RV thrombus .The presence of RV dysfunction or an RV thrombus detected by echocardiography also has prognostic implications.Direct visualization of thrombus is more likely with TEE. Other findings on echocardiography may include inter-ventricular septal flattening with paradoxical motion and loss of respiratory phasic collapse of IVC.
The patient underwent a CT Angiography(Fig 2) which showed-
Multiple intra-luminal filling defects in left and right pulmonary arteries
Main PA - 30 mm
Rt PA - 21 mm
Lt PA - 21 mm
Bilateral pleural effusion
Fig 2: CT angiography showing filling defects in right & left pulmonary artery
What is the value of CT scan in diagnosis of PE?
Â Though pulmonary angiography remains the definitive diagnostic technique or "gold standard" in the diagnosis of acute PE, it is an invasive procedure and so is being replaced with multi detector CT (MDCT) and CT angiography. One of the most commonly cited benefits of CT-PA is its ability to detect alternative pulmonary abnormalities that may explain the patient's symptoms and signs. A negative MDCT in non high clinical probability group almost excludes PE. However in high risk groups, patients with negative MDCT need to undergo further workup. Â One should consider the pretest probability of PE when deciding whether additional diagnostic testing is necessary.
What are the other modalities of imaging PE and DVT?
Pulmonary angiography- A positive pulmonary angiogram provides 100% certainty that an obstruction to pulmonary arterial blood flow does exist. A negative pulmonary angiogram provides greater than 90% certainty in the exclusion of PE. Use of this modality is now restricted only to those cases in which a catheter based intervention is contemplated.
Magnetic Resonance Angiography- A promising modality for the detection in the proximal pulmonary arteries with additional benefit of avoiding iodinated contrast and ionizing radiation. The usefulness of this modality is limited by suboptimal resolution, respiratory and cardiac motion artifact, magnetic susceptibility effects from the adjacent air-containing lung and complicated blood flow patterns. However, there is hope for an expanded role of MRA in the future with new technological advancements.
Ventilation-perfusion (V/Q) scanning - Established test for diagnosis for PE. It is performed by injection of Technetium Tc-99 labeled macroaggregrated albumin particles (perfusion) and inhalation of Xenon-133 gas, Tc-99m labeled aerosols or Tc-99m labeled carbon microparticles (ventilation). VQ mismatch is noted in cases of PE. The largest trial (PIOPED) classified VQ scans into 4 categories- Normal or near normal, low, intermediate (non diagnostic) and high probability of PE. A normal VQ scan in a suspected case almost rules out PE. Non diagnostic scan in a case with low clinical probability is acceptable criteria for ruling out PE.
What is Apcitide scan?
Apcitide scan is a new diagnostic modality that is highly sensitive for imaging acute DVT. 99mTc-apcitide is a radiolabeled peptide, which binds with high affinity and specificity to the glycoprotein IIb/IIIa receptors expressed on the activated platelets that are involved in acute thrombosis. In a recent study it has been found to be more useful compared to contrast venography in patients having no history of DVT or PTE presenting within 3 days of onset of symptoms, with sensitivity of 90.6% and specificity of 83.9%. The data is less compelling for PTE.
What is the role of D-Dimer testing in diagnostic algorithm of PE?
D-dimer test measures the levels of specific degradation products of cross linked fibrin. The sensitivity of this test by ELISA test is reported to be 96-98%, conferring a high negative predictive value. Latex agglutination tests are unreliable, sensitivity being only 50-60% for DVT and PE. This test is best used in conjunction with a clinical assessment scoring system like Well's and Geneva probability scores. A negative test thus excludes PE in patients with low or intermediate pre test probability.
Ischemia-modified albumin is emerging as a potential alternative to D-dimer, the positive predictive value better than D-dimer (93% sensitive and 75% specific for PE).
Patient was thrombolysed using Inj Alteplase and subsequently started on Low molecular weight heparin. He was also continued on Tab Disprin and Atorvastatin.
What is the role of risk stratification in patients with PE?
Patients with suspected acute pulmonary embolism should be stratified as per the risk of an adverse outcome during hospitalization. Risk stratification should be done promptly, since massive pulmonary embolism can be rapidly fatal. Risk stratification is based on clinical features of shock and hypotension (SBP < 90 mm Hg) and markers of myocardial dysfunction or injury (Troponins and BNP). Posthoc analysis of International Cooperative Pulmonary Embolism Registry(ICOPER) data has shown 90 days all cause mortality as 52.4% in patients with SBP<90 mm Hg as compared to 14.7% in patients with SBP> 90 mm Hg. Elevated levels of cardiac Troponins, BNP and NT-proBNP were associated with worse prognosis in patients with suspected PE. Also, right ventricular hypokinesia and dilatation have been shown to be independent predictors of 30-day mortality among hemodynamically stable patients. Risk stratification of patients with PE has clinical implications. The markers of right ventricular dysfunction and injury have a high negative predictive value. Thus, the absence of right ventricular dysfunction and a normal troponin level can identify patients who are eligible for early discharge.
How do you treat established PE?
Acute pulmonary embolism requires initial short term therapy with a rapid-onset anticoagulant which should be initiated while diagnostic confirmation is awaited.
In hemodynamically stable patients, LMWH (Enoxaparin) at a dose of 1 mg per kilogram of body weight given twice daily or Fondaparinux given once daily at a dose of 5 mg for patients weighing less than 50 kg, 7.5 mg for patients weighing 50 to 100 kg, and 10 mg for patients weighing more than 100 kg, are commonly used for the treatment of pulmonary embolism. Intravenous unfractionated heparin (UFH) if used, is given as an initial bolus dose (80 IU per kilogram or 5000 IU), followed by continuous infusion ( starting with 18 IU per kilogram per hour) with adjustment to achieve a target aPTT 1.5 to 2.5 times the normal value. Vitamin K antagonists must be started on the first day and overlap continued till therapeutic INR is achieved.
Hemodynamically unstable patients should be managed with more aggressive treatment, such as pharmacologic thrombolysis or mechanical thrombectomy. This approach is justified by the high rate of death among such patients and by the faster resolution of vascular obstruction with thrombolytics than with only anticoagulant therapy. Mortality in this cohort of patients can be as high as 60% in untreated patients and can be reduced to less than 30% with prompt thrombolysis. A recent meta-analysis showed that i.v. thrombolysis was associated with a reduction in mortality among hemodynamically unstable patients with pulmonary embolism. In hemodynamically stable patients with echocardiographic evidence of right ventricular dysfunction, thrombolysis can be considered. Initial anticoagulation with intravenous unfractionated heparin is appropriate if thrombolytic therapy is being considered. Percutaneous mechanical thrombectomy and surgical embolectomy should be restricted to high-risk patients with absolute contraindications to thrombolysis.
What are the indications and regimes of thrombolysis in patients with PE?
a rapidly acting fibrinolytic agent should be administered immediately to every patient who has suffered hypotension or is hypoxemic from PE
Patients with PE who have any evidence of right heart strain (High Troponin levels) and evidence of RV dysfunction demonstrable by 2-D echo.
rt-PA (alteplase), r-PA (reteplase), urokinase and streptokinase
Alteplase usually is given as an infusion (100 mg over 120 minutes or 0.6 mg/kg over 15 min (max dose-50 mg).
Streptokinase is usually given as infusion over 24 hours or more at a loading dose of 2, 50,000 U, and followed by 1, 00.000 U/ h for 12/24 hours.
Reteplase is given as a single bolus or as 2 boluses administered 30 minutes apart
Shorter infusion of Alteplase has been found to be more effective (and more rapidly effective) than urokinase or streptokinase over a 12-hour period.
What are the predictors of increased mortality in PE?
The factors shown to be associated with a poor prognosis are-
Systolic BP < 100 mmHg
Heart rate > 100/ min
Age > 70 years
Chronic lung disease
Increased natriuretic peptides
RV enlargement on CT chest
What should be the duration of anticoagulation to prevent recurrence of VTE?
The period of long-term anticoagulation should be based on the risk of recurrence after
withdrawal of treatment with vitamin K antagonists and the risk of bleeding. In patients with pulmonary embolism due to a temporary risk factor, therapy with VKAs should be given for 3 months. Patients with unprovoked pulmonary embolism, those with cancer, and those with recurrent unprovoked pulmonary embolism should be treated with indefinite anticoagulation.
First provoked PE
First provoked upper limb DVT
Second provoked VTE
Pulmonary embolism (PE) and deep venous thrombosis (DVT) are two different manifestations of one disease- Venous thromboembolism (VTE). Pulmonary embolism occurs most commonly due to an embolus from the deep vein thrombosis from the legs.
The clinical manifestations range from an asymptomatic presentation to massive embolism leading to death. A high index of suspicion is required in these case as an early diagnosis is essential for institution of effective therapy which may be life saving.
Take home message
Acute pulmonary embolism may mimic acute coronary syndrome and high index of suspicion is required to diagnose this entity.
Early diagnosis and treatment is gratifying while delay or missing massive may be fatal.
Giancarlo Agnelli, Cecilia Becattini, Acute Pulmonary Embolism.N Engl J Med 2010; 363:266-274
Guidelines on the diagnosis and management of acute pulmonary embolism. The Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).European Heart Journal (2008) 29, 2276-2315.
Thrombolytic Therapy for Acute Pulmonary Embolism A Critical Appraisal. Jamie L. Todd, Victor F. Tapson. Chest 2009;135;1321-1329.