NON Q WAVE MYOCARDIAL

INFARCTION

BY- NIRAJ MAHESHWARI, 5TH YEAR

DEPARTMENT OF PROPAEDEUTIC OF INTERNAL DISEASES,
STUDENTS SCIENTIFIC SOCIETY
PERM STATE MEDICAL UNIVERSITY, RUSSIA
WHAT IS MYOCARDIAL INFARCTION?

• A MYOCARDIAL INFARCTION (MI), COMMONLY KNOWN AS A HEART ATTACK,

OCCURS WHEN BLOOD FLOW DECREASES OR STOPS TO A PART OF THE
HEART, CAUSING DAMAGE TO THE HEART MUSCLE.
• THE MOST COMMON SYMPTOM IS CHEST PAIN OR DISCOMFORT WHICH MAY
TRAVEL INTO THE SHOULDER, ARM, BACK, NECK OR JAW. OFTEN IT OCCURS
IN THE CENTRE OR LEFT SIDE OF THE CHEST AND LASTS FOR MORE THAN A
FEW MINUTES. THE DISCOMFORT MAY OCCASIONALLY FEEL LIKE
HEARTBURN.
MAIN CLINICAL CLASSIFICATION OF MI

• THE ELECTROCARDIOGRAM HAS BEEN USED TO CLASSIFY TWO TYPES OF

MYOCARDIAL INFARCTION-
• THE Q-WAVE (TRANSMURAL) INFARCTION, WITH THE IMPLICATION THAT A Q
WAVE REPRESENTS THROUGH-AND-THROUGH ENDOCARDIAL-TO-
EPICARDIAL NECROSIS.
• THE NON—Q-WAVE (NONTRANSMURAL) INFARCTION, WITH THE
IMPLICATION THAT THE ABSENCE OF A Q WAVE INDICATES LESS EXTENSIVE
MYOCARDIAL DAMAGE AND POSSIBLY AN INCREASED POTENTIAL FOR
RECURRENT CORONARY EVENTS.
NON Q WAVE MYOCARDIAL INFARCTION

• A NON-Q WAVE MYOCARDIAL INFARCTION REFERS TO A MYOCARDIAL

INFARCTION THAT DOES NOT RESULT IN A Q WAVE ON THE 12-LEAD ECG
ONCE THE INFARCTION IS COMPLETED.
• IT WAS ONCE BELIEVED THAT THE DEVELOPMENT OF Q WAVES INDICATED
THAT THE INFARCTION WAS “TRANSMURAL” INVOLVING THE FULL
THICKNESS OF THE MYOCARDIUM, HOWEVER AUTOPSY STUDIES FAILED TO
CONFIRM THIS. 
RECENT SCIENTIFIC STUDIES

• ALTHOUGH THE STRATIFICATION OF PATIENTS WITH MYOCARDIAL INFARCTION INTO ECG

SUBSETS BASED ON THE PRESENCE OR ABSENCE OF NEW Q WAVES HAS IMPORTANT
CLINICAL AND PROGNOSTIC UTILITY, SYSTEMATIC EVALUATION OF THE IMPACT OF
THROMBOLYTIC THERAPY ON THE SUBSEQUENT DEVELOPMENT AND PROGNOSIS OF
NON–Q-WAVE INFARCTION HAS BEEN LIMITED TO DATE.
• PATIENTS WERE EXAMINED 12-LEAD ECG, CORONARY ANATOMY, LEFT VENTRICULAR
FUNCTION, AND MORTALITY AMONG 2046 PATIENTS WITH ST-SEGMENT ELEVATION
INFARCTION FROM THE GLOBAL UTILIZATION OF STREPTOKINASE AND TISSUE
PLASMINOGEN ACTIVATOR FOR OCCLUDED CORONARY ARTERIES ANGIOGRAPHIC
SUBSET TO GAIN FURTHER INSIGHT INTO THE PATHOPHYSIOLOGY AND PROGNOSIS OF Q-
VERSUS NON–Q-WAVE INFARCTION IN THE THROMBOLYTIC ERA
RECENT SCIENTIFIC STUDIES

• NON–Q-WAVE INFARCTION DEVELOPED IN 409 PATIENTS (20%) AFTER

THROMBOLYTIC THERAPY. COMPARED WITH Q-WAVE PATIENTS, NON–Q-
WAVE PATIENTS WERE MORE LIKELY TO PRESENT WITH LESSER ST-SEGMENT
ELEVATION IN A NONANTERIOR LOCATION.
CONCLUSIONS AND THE RECENT ADVANCES

• THE STRATIFICATION OF PATIENTS WITH ACUTE MI INTO ECG SUBSETS BY

ABNORMAL NEW Q WAVES HAS IMPORTANT CLINICAL AND PROGNOSTIC
USE. STUDIES IN THE PRETHROMBOLYTIC ERA HAVE SHOWN LOWER IN-
HOSPITAL MORTALITY AMONG PATIENTS WITH NON–Q-WAVE MI. DESPITE A
BETTER INITIAL PROGNOSIS, NON–Q-WAVE MI PATIENTS HAD MORE
FREQUENT INFARCT EXTENSION AND REINFARCTION, RESULTING IN A
SIMILAR OR WORSE LONG-TERM PROGNOSIS COMPARED WITH THOSE WITH
Q-WAVE MI.
SPECIFIC INVOLVEMENT

• ON EXAMINATION OF LEFT VENTRICULAR FUNCTION

• NON–Q-WAVE MI PATIENTS HAD SIGNIFICANTLY BETTER GLOBAL LEFT
VENTRICULAR FUNCTION, AS INDICATED BY GREATER MEDIAN LEFT
VENTRICULAR EJECTION FRACTION, THAN DID Q-WAVE MI PATIENTS
• REGIONAL FUNCTION IN THE INFARCT ZONE WAS ALSO SIGNIFICANTLY
BETTER AMONG NON–Q-WAVE MI PATIENTS
• COMPARED WITH THE Q-WAVE GROUP, THERE WAS A TREND TOWARD LOWER
IN-HOSPITAL MORTALITY AMONG THE NON–Q-WAVE GROUP 
WHY IS THIS CLASSIFICATION NEEDED

• 1) THE Q-WAVE/NON-Q-WAVE DISTINCTION IS USEFUL CLINICALLY, AND

• 2) THE PRIMARY DETERMINANT OF THE PRESENCE OF Q-WAVES IS THE TOTAL
SIZE OF THE UNDERLYING INFARCTION, RATHER THAN ITS TRANSMURAL
EXTENT.
• THUS, THE LARGER THE MI, THE MORE LIKELY Q-WAVES WILL BE PRESENT;
CONVERSELY Q-WAVES ON AN ECG SUGGEST A LARGE INFARCTION AND
LOWER EF.
CLASSIFICATION OF MI IN PRACTISE

• IN ADDITION TO SIGNS SUCH AS CHEST PAIN, A HEART ATTACK IS

DIAGNOSED MAINLY THROUGH 2 WAYS. FIRSTLY IS A BLOOD TEST THAT
SHOWS ELEVATED LEVELS OF CERTAIN MARKERS OF HEART DAMAGE SUCH
AS CARDIAC TROPONIN.
• SECONDLY IS BY LOOKING AT THE ECG HEART TRACING. IF THERE IS A
PATTERN KNOWN AS ST-ELEVATION ON THE EKG, THIS IS CALLED A STEMI,
SHORT FOR ST ELEVATION MYOCARDIAL INFARCTION. IF THERE IS
ELEVATION OF THE BLOOD MARKERS SUGGESTING HEART DAMAGE, BUT NO
ST ELEVATION SEEN ON THE ECG TRACING, THIS IS KNOWN AS A NSTEMI.
NSTEMI MAY BE ASSOCIATED WITH OTHER ECG CHANGES SUCH AS ST
SEGMENT DEPRESSION. OFTEN LOOKING AT THE ECG HELPS US TO LOCATE
THE AREA OF THE HEART THAT IS AFFECTED.
DIFFERENCE IN STEMI AND NSTEMI

• THE BOTTOM LINE IS THAT BOTH ARE JUST AS BAD.

• STEMI IS SEEN AS MORE OF AN IMMEDIATE EMERGENCY BECAUSE THERE IS
A KNOWN TOTAL OCCLUSION OF A HEART VESSEL THAT NEEDS OPENING
BACK UP URGENTLY. IN TERMS OF LONG-TERM OUTCOMES, THEY HAVE
EQUAL HEALTH IMPLICATIONS. PATIENTS WITH NSTEMI OFTEN HAVE OTHER
ILLNESSES SUCH AS ONGOING CRITICAL ILLNESS, DIABETES, KIDNEY
DISEASE, AND OTHER THAT MEANS THEY HAVE A GENERALLY HIGH RISK
OVER THE LONG TERM. BOTH STEMI AND NSTEMI NEED AGGRESSIVE
TREATMENT OVER THE SHORT AND LONG TERM.
EVALUATION

• HISTORY, ECG, AND CARDIAC BIOMARKERS ARE THE MAINSTAYS IN THE

EVALUATION. AN ECG SHOULD BE PERFORMED AS SOON AS POSSIBLE IN
PATIENTS PRESENTING WITH CHEST PAIN OR THOSE WITH A CONCERN FOR
ACS
• A NORMAL ECG DOES NOT EXCLUDE ACS AND NSTEMI. ST-ELEVATION OR
ANTERIOR ST DEPRESSION SHOULD BE CONSIDERED A STEMI UNTIL PROVEN
OTHERWISE AND TREATED AS SUCH. 
EVALUATION

• CARDIAC TROPONIN IS THE CARDIAC BIOMARKER OF CHOICE. TROPONIN IS MORE SPECIFIC AND
MORE SENSITIVE THAN OTHER BIOMARKERS AND BECOMES ELEVATED RELATIVELY EARLY IN THE
DISEASE PROCESS. WHILE CONTEMPORARY CARDIAC TROPONIN MAY NOT BE ELEVATED WITHIN
THE FIRST 2 TO 4 HOURS AFTER SYMPTOM ONSET, NEWER HIGH SENSITIVITY TROPONIN ASSAYS
HAVE DETECTABLE ELEVATIONS MUCH EARLIER.
• IT IS ALSO TRUE THAT THE AMOUNT OF TROPONIN RELEASED, AND THEREFORE THE TIME TO
ELEVATION, IS PROPORTIONAL WITH INFARCT SIZE, SO IT IS UNLIKELY TO HAVE A NEGATIVE INITIAL
TROPONIN WITH LARGER INFARCTS.
• REGARDLESS OF INFARCT SIZE, MOST PATIENTS WITH TRUE ISCHEMIA WILL HAVE ELEVATIONS IN
TROPONIN WITHIN 6 HOURS, AND NEGATIVE TROPONINS AT THIS POINT EFFECTIVELY RULE OUT
INFARCT IN MOST PATIENTS. IN OLDER, CONTEMPORARY TROPONIN ASSAYS, NO DETECTABLE
TROPONIN IS REPORTED IN MOST HEALTHY INDIVIDUALS WITHOUT THE DISEASE. NEWER HIGH
SENSITIVITY TROPONIN ASSAYS OFTEN WILL REPORT A NORMAL DETECTABLE RANGE IN HEALTHY
INDIVIDUALS WITHOUT THE DISEASE.
DIFFERENTIAL DIAGNOSIS
• CLINICAL CONDITIONS THAT CAN PRESENT WITH CHEST PAIN AND HAVE NONSPECIFIC ECG
CHANGES WITH AN ELEVATED TROPONIN MARKER INCLUDE:

• MYOCARDITIS
• PERICARDITIS
• PULMONARY EMBOLISM
• LEFT VENTRICULAR ANEURYSM
• PRINZMETAL ANGINA
• ANXIETY DISORDER
• AORTIC STENOSIS
• HYPERTENSIVE EMERGENCY
TREATMENT DEPENDENCE

• TREATMENT WILL DEPEND ON THE AMOUNT OF BLOCKAGE AND THE SEVERITY OF THE NSTEMI. A
GRACE SCORE WILL DETERMINE WHETHER THE CARDIAC EVENT IS LOW, MEDIUM, OR HIGH RISK.
THIS SCORE USES THESE EIGHT PARAMETERS TO CALCULATE RISK:

• AGE
• HEART RATE
• SYSTOLIC BLOOD PRESSURE
• KILLIP CLASS (PHYSICAL EXAMINATION)
• SERUM CREATININE LEVEL
• CARDIAC ARREST AT HOSPITAL ADMISSION
• ST-SEGMENT DEVIATION IN ECG
• ELEVATED CARDIAC MARKER
TREATMENT DEPENDENCE

• MEDICATIONS THAT MAY BE GIVEN INCLUDE ANTICOAGULANTS,

ANTIPLATELETS, BETA-BLOCKERS, NITRATES, STATINS, ANGIOTENSIN-
CONVERTING-ENZYME (ACE) INHIBITORS, OR ANGIOTENSIN RECEPTOR
BLOCKERS (ARBS).
THANK YOU