Practical Cardiovascular Medicine. Elias B. Hanna

upper sternal borderRVright ventricle/ventricularRVADright ventricular assist deviceRVEDPright ventricular end-diastolic pressureRVHright ventricular hypertrophyRVOTright ventricular outflow tract SA sinoatrialSA O2systemic arterial oxygen saturationSAMsystolic anterior motionSaO2systemic arterial oxygen saturationSBEsubacute bacterial endocarditisSBPsystolic blood pressureSCDsudden cardiac deathSGLT-2inhibitor sodium-glucose cotransporter-2 inhibitorSIRSsystemic inflammatory response syndromeSFAsuperficial femoral arterySNRTsinus node reentrant tachycardiaSPECTsingle photon emission computed tomography (nuclear imaging)SQsubcutaneouslySTEMIST-segment elevation myocardial infarctionSTSSociety of Thoracic SurgeonsSVstroke volumeSVCsuperior vena cavaSVGsaphenous venous graftSvO2mixed venous oxygen saturation (also MV O2)SVRsystemic vascular resistanceSVTsupraventricular tachycardiaTAAthoracic aortic aneurysmTdPtorsades de pointesTEEtransesophageal echocardiogramTGstriglyceridesTGAtransposition of great arteriesTIAtransient ischemic attackTIDtransient ischemic dilatationTRtricuspid regurgitationTSHthyroid stimulating hormoneTTEtransthoracic echocardiogramUAunstable anginaUFHunfractionated heparinVADventricular assist deviceV/Qscan lung ventilation/perfusion scanVFventricular fibrillationVLDLvery-low-density lipoproteinVpvelocity of propagationVSDventricular septal defectVSRventricular septal ruptureVTventricular tachycardiaVTIvelocity-time integralWPWWolff–Parkinson–White

About the Companion Website

      This book is accompanied by a companion website.

      www.wiley.com/go/hanna/practicalcardiovascularmedicine

      This website includes:

       Multiple choice questions

Part 1 CORONARY ARTERY DISEASE

      1

      Non-ST-Segment Elevation Acute Coronary Syndrome

        I. Definition, types of myocardial infarction, and pitfalls

        II. Clinical features, ECG, cardiac biomarkers, and echocardiography in ACS

        III. Initial approach to acute chest pain presentations and the use of conventional and high-sensitivity troponins

        IV. Management of NSTEMI

        V. General procedural management after coronary angiography: PCI, CABG, or medical therapy only

        VI. Discharge medications in NSTEMI

        VII. Prognosis

        Appendix 1. Complex angiographic disease- Moderate disease progression

        Appendix 2. Women and ACS, elderly patients and ACS, CKD

        Appendix 3. Bleeding, transfusion, patients on chronic warfarin or NOAC, gastrointestinal bleed

        Appendix 4. Antiplatelet and anticoagulant therapy

        Appendix 5. Difference between plaque rupture and plaque erosion

        Appendix 6. Spontaneous coronary artery dissection

        Appendix 7. Harmful effects of NSAIDs and cyclooxygenase-2 inhibitors in CAD

        Appendix 8. Additional ideas on the physiology of hs-troponin-Role of hs-troponin in primary prevention

        Questions and answers

I. Definition, types of myocardial infarction, and pitfalls

A rise in troponin, per se, is diagnostic of myocardial necrosis or injury but is not sufficient to define myocardial infarction (MI), which is myocardial necrosis secondary to myocardial ischemia. Additional clinical, ECG, or echocardiographic evidence of ischemia is needed to define MI (Figure 1.1).

      In fact, MI is defined as a troponin elevation above the 99th percentile of the reference limit (~0.03 ng/ml, depending on the assay) with a rise and/or fall pattern, along with any one of the following four features: (i) angina; (ii) new or dynamic ST-T abnormalities not explained by LVH or LBBB, or new Q waves; (iii) new wall motion abnormality on imaging; (iv) intracoronary thrombus on angiography.^1,2

      Isolated myocardial necrosis is common in critically ill patients and manifests as a troponin rise, sometimes with a rise and fall pattern, but no clinical or ECG features of MI. This troponin rise is not called MI but is called “non-MI troponin elevation” or “non-ischemic myocardial injury”.

      A rise or fall in troponin is necessary to define MI. A mild, chronically elevated but stable troponin may be seen in chronic heart failure, severe left ventricular hypertrophy, or advanced kidney disease. While having a prognostic value, this stable troponin rise is not diagnostic of MI. A fluctuating troponin pattern may be seen in myocarditis. Different cutoffs have been used to define a relevant troponin change, but, in general, a troponin that rises above the 99th percentile with a rise or fall of > 20% is characteristic of MI (50-80% cutoff is more applicable to low troponin levels <0.1 ng/ml).³

      A .Type 1 MI (spontaneous MI) = True acute coronary syndrome (ACS)

      Type 1 or spontaneous MI is usually due to plaque rupture or erosion that promotes platelet aggregation, thrombus formation and microembolization of platelet aggregates.

NSTEMI is a type 1 MI without persistent ST-segment elevation. STEMI is a type 1 MI with persistent (> 20 min), ischemic ST-segment elevation.^1,4 For practical purposes, ischemic symptoms with ongoing ST-segment elevation of any duration are considered STEMI and treated as such. The diagnosis may be retrospectively changed to NSTEMI if ST elevation quickly resolves without reperfusion therapy, in < 20 minutes.