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for the management of acute coronary syndrome, echocardiography in acute coronary syndrome, use of radionuclide imaging in acute coronary syndrome, computed tomographic angiography in acute cardiac care
Acute Aortic Syndrome INTRODUCTION Acute aortic syndrome (AAS) represents a spectrum of life-threatening conditions with similar clinical presentation and the need for urgent management It includes classic acute aortic dissection (CAAD), intramural hematoma (IMH), and penetrating aortic ulcer (PAU) Although not included in the original definition of AAS, traumatic aortic rupture (TAR) and aortic aneurysm rupture have also been considered to be part of the AAS spectrum AAS is characterized by disruption of the media layer of the aorta and typically presents with acute chest pain The term “acute aortic syndrome” was first coined in 2001 by the Spanish cardiologists Vilacosta and San Román, who described AAS as a spectrum of interlinked lesions1 with the intent to increase awareness and to speed up diagnosis and appropriate treatment (Figure 32.1) FIGURE 32.1 Acute aortic syndrome The acute aortic syndrome triad first described by Vilacosta and San Román Arrows signify possible progression of aortic lesions (penetrating aortic ulcer to IMH, penetrating aortic ulcer to classic dissection, IMH to classic dissection) IMH, intramural hematoma Although the incidence of AAS is lower than that of acute coronary syndrome (ACS), AAS carries a higher mortality, and is therefore a critical component of the differential diagnosis of chest pain in the Cardiac Care Unit (CCU) Overall incidence of AASs is 2 to 4 cases per 100,000 individuals Because AAS is rare, the International Registry of Acute Aortic Dissection (IRAD) was created in 1996 as a way to combine data acquired from multiple top institutions in Europe, North America, and Asia.2 The 2010 intersocietal guidelines for the diagnosis and management of patients with thoracic aortic disease proposed a standard approach to the diagnosis and treatment of AAS.3 Although clinical history and physical examination are important, imaging is essential in the diagnosis of AAS Transesophageal echocardiography (TEE), computed tomography (CT), and magnetic resonance imaging (MRI) are the preferred imaging modalities and angiography is rarely needed CLASSIFICATION OF ACUTE AORTIC SYNDROMES Historically, CAAD was the first recognized form of AAS The classification schemes used for the classic aortic dissection were subsequently extended to include IMH and PAU AASs are classified on the basis of the location and extent of involvement of the aorta Two systems have been proposed, the DeBakey and the Stanford systems (Figure 32.2) The DeBakey system, which was proposed in 1965 by the Lebanese-American surgeon Michael Ellis DeBakey, divided aortic dissection into three types based on the anatomic location Type I originates in the ascending aorta and propagates beyond the aortic arch, type II is limited to the ascending aorta only, and type III is limited to the descending aorta.4 FIGURE 32.2 DeBakey and Stanford classifications Left: DeBakey classification of aortic dissection Type I includes the ascending and descending aorta, type II includes the ascending aorta only, and type III includes the descending thoracic aorta only (DeBakey ME, Henly WS, Cooley DA, et al Surgical management of dissecting aneurysms of the aorta J Thorac Cardiovasc Surg 1965;49:130-149.) Right: Stanford classification Type A aortic dissection involves the ascending thoracic aorta, and type B involves the descending thoracic aorta only All three AAS conditions; CAAD, IMH, and PAU use the Stanford classification CAAD, classic acute aortic dissection; IMH, intramural hematoma; PAU, penetrating aortic ulcer (Daily PO, Trueblood HW, Stinson EB, et al Management of acute aortic dissections Ann Thorac Surg 1970;10[3]:237-247.) The Stanford system, which was created by researchers at Stanford University in 1970, divides aortic dissections into two types Type A includes any dissection that involves the ascending aorta, whereas type B dissections are limited to the descending thoracic aorta.5 The Stanford classification appears to have wider acceptance and is now used for all three AAS types: CAAD, IMH, and PAU INTRAMURAL HEMATOMA IMH is defined by crescentic or circumferential thickening of the media layer of the aortic wall IMH is likely due to a ruptured vasa vasorum resulting in intramural bleeding but without a detectable intimal tear It was first described in 1920 by the German pathologist Ernst Kruckenberg, who is also well known for his description of the so-called Kruckenberg tumors (transperitoneal ovarian metastases from stomach and colon cancers) On TEE, CT, or MRI, IMH is typically visualized as a crescentic or concentric thickening of the aortic wall > 5 mm (Figure 32.3) The natural history of IMH often includes progression to CAAD, which accounts for its high morbidity and mortality FIGURE 32.3 Intramural hematoma: CT CT of the chest shows the descending thoracic aorta The crescentic-shaped lesion on the patient’s left signifies an IMH (dashed arrows) CT, computed tomography; IMH, intramural hematoma Etiology and Pathophysiology IMH may account for up to 6% to 30% of all AAS, with a higher reported prevalence among the Korean and Japanese populations as compared with Western subjects.6 It is unclear whether this is a true discrepancy in prevalence versus a reflection of differing classification, evaluation, or treatment practices Often, IMH is diagnosed as such even though very small intimal tears indicative of limited aortic dissection may be present but missed by modern imaging modalities This may overestimate the true prevalence of IMH as opposed to CAAD The characteristic feature of IMH is its location in the portion of the media closer to the adventitia, as opposed to CAAD which is typically located in the media closer to the intima Although the most cited hypothesis of the pathophysiologic mechanism of IMH is rupture of the vasa vasorum, there is very little corroborating clinical or experimental evidence Owing to the low incidence of IMH and the close association with CAAD, a definitive etiology still remains unclear.7 Clinical Manifestations According to the IRAD experience, IMH typically presents with the symptoms of severe chest and back pain, similar to CAAD However, IMH is less likely to present with manifestations of severe aortic regurgitation and pulse deficits.6 IMH is rarely stable It may either progress to CAAD or regress spontaneously, and therefore serial imaging is crucial Stanford type B lesions in the descending aorta are more common than type A lesions in the ascending aorta (60% vs 35% of all IMH, respectively) Cardiogenic shock may be present in 14% of patients, more typically with type A IMH.8 Pericardial effusion and tamponade may also be present, which are also more common in type A IMH When compared with CAAD, type A IMH has a significantly higher risk of rupture (26% vs 8%, respectively).9 A widened mediastinum may be present on chest X-ray; however, this is neither sensitive nor specific to IMH Diagnosis As with all types of AAS, rapid diagnosis is paramount in IMH TEE, CT, and MRI are the preferred diagnostic tools CT is often chosen because of widespread availability, rapid acquisition, and its ability to diagnose other causes of acute chest pain such as trauma and pulmonary embolism Classically, absence of an intimal flap or tear differentiates IMH from CAAD Often, IMH can be identified even on non–contrast-enhanced CT On contrast CT scans, a crescentic or circular area of high attenuation that does not enhance with contrast is present Similar findings are seen on MRI, which has the advantage of not requiring iodinated contrast On TEE, IMH is diagnosed if there is regional thickening of the aortic wall > mm in a crescentic or circumferential pattern without an intimal flap or tear (Figure 32.4A, B) Limitations of TEE in diagnosing IMH arise from the TEE’s inability to visualize all portions of the aorta including the area around the origin of the brachiocephalic artery and all but the most proximal portions of the abdominal aorta TEE is very useful in diagnosing complications of IMH, such as pericardial effusion or aortic regurgitation FIGURE 32.4 Intramural hematoma: TEE Two-dimensional (2D) TEE of the ascending thoracic aorta in the long-axis (A) and short-axis (B) views Yellow arrows point to a crescentic thickening of the anterior portion of the ascending thoracic aortic wall, consistent with a type A IMH IMH, intramural hematoma; TEE, transesophageal echocardiography Small intimal tears may be missed by any modern imaging technique, challenging the diagnosis of classic IMH Management and Prognosis The prognosis of IMH is somewhat better than that of CAAD As in all AAS, the main determinant of prognosis is its aortic location According to the IRAD registry, the mortality of type A IMH is approximately 27%, compared with 4% in type B IMH Invasively managed patients with type A IMH typically fare better than medically managed patients Invasive options include open surgical repair and percutaneous thoracic endovascular aortic repair Medical management typically consists of heart rate (HR), blood pressure, and pain control Surgical mortality for IMH is similar to that for other forms of AAS Type B IMH is often managed medically Approximately 50% of type B patients may improve with medical management alone, 15% will remain stable, and 35% may progress to aneurysm formation, CAAD, or focal aortic rupture (pseudoaneurysm).10 Intramural Hematoma in Pregnancy Although there are no specific guidelines in pregnancy for patients with IMH, pregnancy is considered a risk factor for the development of aortic pathology, especially in Marfan syndrome As with other forms of AAS, expedited delivery via caesarian section is considered reasonable for pregnant patients with acute IMH, if possible CLASSIC ACUTE AORTIC DISSECTION CAAD is the most common form of AAS.2 It occurs in approximately 66% to 75% of all AAS The overall incidence of CAAD is low, estimated at 0.5 to 4.0 cases per 100,000 per year, and is thought to affect men more than women in a 2:1 ratio Risk factors for CAAD include connective tissue disorders such as Marfan (fibrillin gene), Loeys–Dietz (transforming growth factor β receptor and genes), Ehlers–Danlos type (collagen gene), and Turner syndrome (X monosomy), as well as the aortopathy associated with bicuspid aortic valve (NOTCH1 gene) In addition, hypertension is a significant risk factor and is more prevalent among older patients Last, aortic instrumentation or surgery, as well as cardiac catheterization, are rare but reported causes of aortic dissection CAAD was first described in 1555 by Andreas Vesalius (1514–1564) who reported traumatic abdominal aortic aneurysm in a man who fell off a horse.11 Intimal tear, the hallmark of CAAD, was first described by Daniel Sennert (1572–1637), a German anatomist and published in 1650 posthumously.12 A very famous description of CAAD was by the British royal physician Frank Nichols (1699–1778) who provided the first unmistakable account of CAAD (deemed a “Transverse fissure of the aortic trunk”) in his autopsy of King George II, who died in 1760 while straining in the lavatory Successful surgical repair of descending aortic dissection was not reported until 1955, by Michael Debakey (1908–2008) and his colleagues, and ascending dissection until 1962 by Frank Spencer and Hu Blake.13,14 Etiology and Pathophysiology CAAD is characterized by an intimal tear, which leads to abnormal blood flow from the aortic lumen into the media (Figure 32.5) Consequently, there is a longitudinal separation of the media layers by the blood flow, which tears an intimomedial flap from the remainder of the aortic wall (Figure 32.6A–C) This flap separates the abnormal false lumen from the true aortic lumen Intimal tears typically occur at the locations within the aorta with the highest shear stress These are at the right side of the ascending aorta immediately distal to the ostium of the right coronary artery (type A dissections) and immediately distal to the ostium of the subclavian artery adjacent to the insertion of the ligamentum arteriosus (type B dissections) San Francisco Syncope Rule (SFSR), 285 Sarcoidosis CD4+-mediated disease, 171 LGE-CMR technology, 171–172 positron emission tomography, 172, 172f systemic non-necrotizing granulomatous, 171 and ventricular arrhythmia, 281 Sarcomeric mutation in HCM, 149 Saturated fats, 708 SB See Sinus bradycardia SCD See Sudden cardiac death Seagull sign, 619 Seashore sign, 609t, 611, 612f Seat belt sign, 368 Secundum atrial septal defect, 452–453 Sedation Agitation Scale (SAS), 489t Sedatives and analgesic medications addiction, 501 arterial and central venous lines, 496 breathing tube, 503 catheters and device insertion, 502–503 delirium, 501 desired and precise level, 488 direct current cardioversion, 495, 502 Glasgow Coma Scale, 489 hypnotics, 492–493 intra-aortic balloon pump, 496 opioids, 490–492 pain assessment, 488 pain management, 499–500 pain medications, 500 pericardiocentesis, 495–496 Ramsay Sedation Scale, 489, 489t Richmond Agitation–Sedation Scale, 489, 490t Sedation Agitation Scale, 489t sleep medications, 500–501 temporary transvenous pacing, 496 transesophageal echocardiography, 495, 502 upper GI endoscopy, 496 Sedentary behavior, 703, 704f Seldinger technique, 568 Selective serotonin reuptake inhibitors (SSRIs), 357 SELF pathway, 285, 287f Serotonin norepinephrine reuptake inhibitors (SNRIs), 357 Sheath introducer, 543f, 544 SHIFT See Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial, 18, 141, 141t, 144 Shred sign, 609t Sildenafil drug-induced liver injury, 535t HFpEF, 121 Simpson’s rule analysis, 33 Single photon emission computed tomography myocardial perfusion imaging (SPECT MPI) fixed perfusion defect, 43, 45f heart attack, 47 homogeneous tracer uptake, 43, 44f low-risk patients, 46 myocardial radiotracer uptake, 41, 42f orientations, 43, 43f post–myocardial infarction, 46 radiotracers, 41, 43, 45 resting SPECT MPI protocols, 43, 45 reversible perfusion defect, 43, 44f SPECT camera, 41 stress testing, 43 viability assessment, 43, 45 Single-dose epinephrine (SDE), 323 Sinoartrial node (SAN) blood supply, 226 conduction, 226 sinus rhythm, 226 Sinoatrial exit block, 228 Sinotubular junction (STJ), 437 Sinus arrhythmia definition, 226 differential diagnosis, 226 mechanism, 227 nonrespiratory, 226–227 respiratory, 226 ventriculophasic, 227 Sinus bradycardia (SB) ACLS adult bradycardia algorithm, 233, 233f asymptomatic, 226, 228 causes of, 228t, 238 diagnosis, 238 heart rate, 226, 233 hemodynamic compromise, 233 increased vagal tone, 227, 227f infectious agents, 228 metabolic derangements, 228 obstructive sleep apnea, 228 pacemaker, 238 permanent pacemaker, 236–237 physiologic, 226 symptomatic, 228 symptoms, 226, 238 systolic blood pressure, 233 temporary pacing, 233–234 transcutaneous pacing, 234, 234f transvenous pacing, 234–236, 235f treatment, 238 Sinus node dysfunction (SND) bradycardia See Sinus bradycardia sinus pause/arrest, 228 syncope, 289 treatment, 228 Sinus pause/arrest, 228 Sinus rhythm, 226 Sinus tachycardia, 239 Sinusoid sign, 609t Situational syncope, 292 Sleep apnea behavioral treatment options, 217 central sleep apnea, 215–216 factors predisposing, 224 obstructive sleep apnea, 215–217 patient education program, 220t Sleep Apnea Pathway, 217 Sleep Apnea Pathway (SAP), 217, 218t Smoking, 700, 700f Smoking cessation, 683, 692–693 behavioral modification, 689, 693 bupropion, 687–688 CO, 684 coagulation and hemostasis abnormalities, 684 endothelial dysfunction, 684 mechanism, 683, 683f nicotine addiction, 684–685, 684f NRT See Nicotine replacement therapy oxidative stress, 683 pharmacotherapy, 689 principles involved, 689–690 systemic inflammation, 683–684 varenicline, 688–689 SMVT See Sustained monomorphic ventricular tachycardia SND See Sinus node dysfunction Social support, 736 Society of Thoracic Surgeons predicted operative mortality score (STS-PROM) score, 421, 437 Sodium, 710 Sodium channel blockade disopyramide, 335 flecainide, 337, 343 lidocaine, 337 mexilitine, 337 pill-in-the-pocket approach, 337 procainamide, 335–337 propafenone, 337, 343 quinidine, 335 Sodium nitroprusside, 75, 638 Somatosensory evoked potentials (SSEPs), 517–518 SonR-closed-loop optimization, 303, 304f Sorin Orchestra Plus programmer, 309, 309f Sotalol, 339, 343–344 SPECT MPI See Single photon emission computed tomography myocardial perfusion imaging Spectral Doppler, 365 Sphygmomanometer, 375 Spinal blood clots, 359–360 Spironolactone heart failure treatment, 205t, 206, 207 HFpEF, 121 hypertension, 636 STEMI, 16 Splenomegaly, 414 Spontaneous breathing trial (SBT), 78 SSEPs See Somatosensory evoked potentials St Jude Medical Merlin programmer, 307, 307f Stable ischemic heart disease (SIHD), 53 Standardized ISHLT Cardiac Biopsy Grading Scales, 198t Static air bronchograms, 609t Statins drug-induced liver injury, 535t LDL reduction, 29, 681 lipid management beneficial mechanisms, 675 contrast-induced acute kidney injury, 675 early treatment effects, 673–674 in endothelial dysfunction, 697 intolerance and adverse effects, 675 PCI, 675 therapy intensity and LDL-C reduction, 676, 676t STEMI, 16 stroke, 528 sudden cardiac death, 312 STEMI See ST-segment elevation myocardial infarction Stented valves, 446 Stratosphere sign, 609t, 611, 612f Strength training, 724, 724t Strength-duration curve, 300, 301f Streptokinase (SK), 92, 92t Stress cardiomyopathy, 695, 695f, 698 See also Takotsubo cardiomyopathy echocardiography exercise testing, 36 myocardial ischemia, 25 pharmacologic stress echocardiogram, 36 risk stratification, 36–37 stress inducing methods, 36t management, 736–737, 737f myocardial perfusion imaging, 43 exercise, 43 fixed perfusion defect, 43, 45f homogeneous tracer uptake, 43, 44 low-risk patients, 46 pharmacologic stress testing, 43 post–myocardial infarction, 46 testing, 695 Stress-rest myocardial perfusion, 701, 701f Stroke anticoagulation antiplatelet therapy, 255 bleeding risk assessment, 255t CHA2DS2-VASc score, 269 HAS-BLED score, 269 LAA occlusion, 255–256, 257f novel oral anticoagulants, 255 vitamin K antagonist, 255 aortic valve replacement, 438 CHA2DS2-VASc score, 345–346, 346t CT scan, 528 CTA, 528 HAS-BLED score, 346, 346t, 347f hemorrhagic, 528 hypertension ischemic, 528 See also Ischemic stroke magnetic resonance angiography, 528 medications, 528 mitral valve surgery, 443 MRI, 528 obstructive sleep apnea, 216–217 rehabilitation, 528 symptoms, 528 transcatheter aortic valve replacement, 424 Stroke Prevention in Atrial Fibrillation-1 (SPAF-1), 356–357 Stroke volume (SV), 110 Stroke volume variation (SVV), 586 ST-segment elevation myocardial infarction (STEMI) acute coronary syndrome, 162 biomarkers, 10–11 cardiogenic shock, 141 coronary angiography, 16 discharge planning, 19 echocardiography, 16 electrocardiogram, 9–10, 10f epidemiology, 9 fibrinolytic therapy, 12, 13t, 82 medical management ACE inhibitors, 16 aldosterone antagonists, 16 anticoagulant therapy, 15 antiplatelet therapy, 13–15 β-blockers, 15–16 statin therapy, 16 pathophysiology, 9 percutaneous coronary intervention, 59 postoperative complications atrioventricular block, 18 bleeding, 17 cardiogenic shock, 18–19, 18t left ventricular aneurysm, 18 left ventricular rupture, 17 left ventricular thrombus, 18 mitral regurgitation, 17 ventricular arrhythmia, 18 primary PCI, 12 risk assessment, 11–12 stress testing, 16–17 symptoms, 9 system of care, 12 Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments (SUPPORT), 624 Sudden cardiac death (SCD) adult congenital heart disease, 458–459 antiarrhythmic drugs, 312 arrhythmia pathophysiology, 311 β-blockers, 312 coronary angiography, 53 CRT See Cardiac resynchronization therapy definition, 311 ESCAPE pathway See ESCAPE pathway hypertrophic cardiomyopathy, 171, 171f ICD See Implantable cardioverter defibrillator NSVT prediction, 273 risk factors, 311 risk stratification, 311–312 statins, 312 ventricular arrhythmias, 170–171 Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), 312, 313 Sufentanil, 491 Supra-aortic angiography, 58 Supraventricular tachycardia (SVT) ablations, 251 beta-blockers, 251 calcium channel blockers, 251 carotid sinus massage, 250 electrical cardioversion, 250 electrocardiogram, 239 electrophysiology study, 250, 251 heart rate, 250 incidence, 239 IV adenosine, 251 vs sinus tachycardia, 250 symptoms, 250 vagal maneuvers, 250 and ventricular tachycardia (VT), 275, 275t Surface cooling, 329–330 Surgical aortic valve replacement (SAVR), 390, 391 Surgical tamponade, 375 Sustained monomorphic ventricular tachycardia (SMVT), 276, 277f, 277t Sustained polymorphic ventricular tachycardia, 276, 278, 278f Sustained release (SR), 687, 688 SVR See Systemic vascular resistance SVT See Supraventricular tachycardia Swan-Ganz catheterization See Pulmonary artery catheter SWORD trial, 339 Synchronized intermittent mandatory ventilation (SIMV), 78 Syncope cardiac event monitoring, 288 classification, 285 definition, 285, 292 echocardiography, 286, 288 electrocardiogram, 286, 292 electrophysiologic testing, 289, 293 exercise testing, 288–289 Holter monitoring, 288 implantable cardioverter defibrillator, 293 implantable loop recorders, 289, 289f, 290f, 293 initial assessment, 285, 288t, 292 pericardial disease, 382, 383f, 383t, 384f permanent pacemaker, 293 physical examination and laboratory testing, 292 principle causes, 285, 286t risk stratification, 285–286 SELF pathway, 285, 287f tilt-table testing, 289, 292–293 Systemic inflammation, 683–684 Systemic vascular resistance (SVR), 75, 143, 584, 584t, 585t Systolic anterior motion (SAM) of mitral valve, 151, 151f, 155 myectomy, 154 persistent, 154 residual, 154 Systolic blood pressure, 375 Systolic Blood PRessure INTervention (SPRINT) trial Systolic function assessment aortic stenosis, 433 non-ST-elevation myocardial infarction, 32 ST-elevation myocardial infarction, 32 ventricular ejection fraction, 33 wall motion scoring analysis, 32 Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial (SHIFT), 210 T Tachyarrhythmia CMR imaging, 161 heart transplantation, 195 syncope, 286 Tachycardia atrial tachycardia See Atrial tachycardia coronary artery bypass surgery, 74 HFrEF, 110 pericardial tamponade, 375 therapy devices, 302–303 ventricular tachycardia See Ventricular tachycardia Tacrolimus, 197 Tai chi, 724 Takotsubo cardiomyopathy acute LVOT obstruction, 156–157 apical ballooning, 169 cine imaging, 169, 170f invasive/noninvasive angiography, 169 low-intensity LGE, 169, 170f myocardial infarction and myocarditis, 169, 170t women’s heart disease, 695, 695f, 698 Tamponade See also Pericardial effusion and tamponade acute, 75, 75t, 375 TandemHeart percutaneous assist device clinical use, 184, 184f complications, 184 device size, 183t hemodynamic effects, 183t vs IABP, 184 indications, 184–185 insertion, 183t mechanism of action, 183t TAR See Traumatic aortic rupture Targeted temperature management (TTM) acute neurologic emergencies, 518 Bayes’ theorem, 329, 329f cooling phase, 325, 327f, 328 degree of postarrest brain injury, 328–329, 329f endovascular vs surface cooling, 329–330 neurologic prognosis, 328 normothermia phase, 327f, 328 pathway, 324, 326f post-cardiac arrest care, 330 presentation to emergency department, 324–325, 327f rewarming phase, 327f, 328 TAVR See Transcatheter aortic valve replacement Technetium-99m (Tc-99m), 43 TEE See Transesophageal echocardiography Tenecteplase (TNK), 92–93, 92t Tense-tiredness, 734 Tetralogy of Fallot (TOF), 281, 455–456 TH See Therapeutic hypothermia The Complete versus Culprit-only Revascularization to Treat Multi-vessel Disease After Primary PCI for STEMI (COMPLETE) trial 4, 17 The Trial of Routine Angioplasty and Stenting after Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction (TRANSFER-AMI) study, 16 The Triple Therapy in Patients on Oral Anticoagulation After Drug Eluting Stent Implantation ((ISARTRIPLE), 256 Theophylline dosage, 234t mechanism of action, 234t side effects, 234t Therapeutic hypothermia (TH) history, 324 targeted temperature management Bayes theorem, 329, 329f cooling phase, 325, 327f, 328 degree of postarrest brain injury, 328–329, 329f endovascular vs surface cooling, 329–330 neurologic prognosis, 328 normothermia phase, 327f, 328 pathway, 324, 326f post-cardiac arrest care, 330 presentation to emergency department, 324–325, 327f rewarming phase, 327f, 328 Thermodilution, 583–584 Thiazide diuretics, hypertension, 636 Third Danish Study of Optimal Acute Treatment of Patients with ST-Segment Elevation Myocardial Infarction (DANAMI 3-PRIMULTI) trial, 17 Thoratec Heartmate II Left Ventricular Assist Device (HM-II LVAD), 187, 188f Threshold testing, 300–301, 301f Thrombectomy, 64 Thromboembolic complications (TEC), 348 Thromboembolism aortic valve replacement, 438 mitral valve surgery, 443 Thrombolysis in myocardial infarction (TIMI) risk score, 11, 26, 163 Thyroid, renal failure, anemia, pulmonary disease and sepsis (TRAPS), 102 Ticagrelor acute coronary syndrome, 88 MI and stent thrombosis risk reduction, 27–28 STEMI, 15 Ticlopidine, 535t Tidal volume, 468 Tilting disc valves, 446 Tilt-table testing, 289, 292–293 Tirofiban, 89 Tissue echogenicity, 603, 603t, 604f Tissue plasminogen activator (t-PA), 684 Tolvaptan, 535t Torsades de pointes (TdP), 278, 278f, 340, 340t TR See Tricuspid regurgitation Trabecular ventricular septal defect, 453 Trans fat, 708 Transcatheter aortic valve replacement (TAVR) aortic regurgitation, 387, 393 aortic stenosis, 387, 390–391, 391f, 450 caval-aortic, 424 conduction system disease, 424 coronary ostia occlusion, 424 echocardiography and fluoroscopy, 423f Edwards S3 and Sapien XT valves, 423, 424 intraprocedural complications, 424 leaflet thrombosis, 424 life expectancy, 422 myocardial infarction, 424 paravalvular leak, 424 patient selection, 422 risk assessment, 422 stroke, 424 survival, 421, 424 transfemoral, 424 valve-in-valve TAVR, 423 Transcatheter mitral valve replacement (TMVR), 427–428 Transcatheter pulmonary valve replacement, 428 Transcatheter tricuspid valve intervention, 428 Transcutaneous pacing, 74, 234, 234f Transeptal puncture, 184 Transesophageal echocardiography (TEE) acute coronary syndrome, 40 aortic stenosis, 387, 387f atrial fibrillation, 254 cardiopulmonary bypass, 71 hypertrophic cardiomyopathy, 156 infective endocarditis, 414, 415f mitral regurgitation bileaflet mitral valve endocarditis, 402f eccentric paravalvular, 404f myxomatous mitral valve, 403f prosthetic valve endocarditis, 404f mitral valve stenosis, 397, 398f, 400 pericardial effusion and tamponade, 374 sedatives and analgesic medications, 495 tricuspid regurgitation, 409f Transthoracic echocardiography (TTE) acute decompensated HCM, 156 atrial septal defect, 452 classic acute aortic dissection, 366 coarctation, 455 hypertrophic cardiomyopathy, 151, 151f infective endocarditis, 414, 415f mitral regurgitation bileaflet mitral valve endocarditis, 402f papillary muscle rupture, 403f mitral valve stenosis, 399, 400 myocardial rupture, 125, 125f pericardial effusion and tamponade, 373 ventricular septal defect, 453 Transvenous pacing wires, 74 Traumatic aortic rupture (TAR) in acute aortic syndrome, 372 clinical manifestations, 368 diagnosis, 368–369, 369f etiology and pathophysiology, 368 management and prognosis, 369 pregnancy, 369 Traumatic tricuspid valve rupture, 444 Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with PrasugrelTIMI (TRITON-TIMI), 14, 28 Tricuspid annular (TA) dilatation, 407 Tricuspid regurgitation (TR) clinical findings, 444 clinical presentation, 407 diagnosis, 407–408 etiology and pathophysiology, 407, 407t, 408f, 409f medical therapy, 408 morphology, 444 pregnancy, 412 surgical therapy, 408–409, 412 transcatheter tricuspid valve intervention, 428 tricuspid valve surgery, 444 Tricuspid ring annuloplasty, 441 Tricuspid stenosis (TS), 409, 410f Tricuspid valve (TV) endocarditis, 407 Triglycerides, 680 Trileaflet aortic valve (TAV), 387 Triple lumen catheter, 543f, 543t, 544, 573 Triple rule out protocol, 48 Troponins myocardial damage, 41 STEMI, 9 True left ventricular aneurysm See Left ventricular aneurysm (LVA) Trypanosoma cruzi, 200 TTE See Transthoracic echocardiography TTM See Targeted temperature management Tubular necrosis, acute, 510 Tubular obstruction, 506 Turbulent flow, 433 U Ultrafiltration, 104 Ultrasound, 620–621, 621f See also Point-of-care ultrasound; Abdominal ultrasonography arterial line placement, 569–570 central venous catheters, 550–552 kidney failure, 513 Unfractionated heparin (UFH) availability, 483t acute coronary syndrome, 90 modern anticoagulation therapy, 346 non–ST-elevation myocardial infarction, 28 percutaneous coronary intervention, 62 United Kingdom National Cardiac Arrest Audit database, 320 United States Food and Drug Administration (US FDA), 345 UNload the Left ventricle in patients with ADvanced heart failure (UNLOAD) trial, 206 Unstable angina (UA), 82 Upper limit of normal (ULN), 675 U.S Clinical Practice Guidelines for Treating Tobacco Use and Dependence, 685 U.S Department of Health and Human Services, 688 US Food and Drug Administration, 322 Uvulopalatopharyngoplasty (UPPP), 220, 224 V VA See Ventricular arrhythmia VAD See Ventricular assist device VA-ECMO See Venoarterial extracorporeal membrane oxygenation Vagal atrioventricular block, 230, 230f Vagal maneuvers atrial tachycardia, 247 AVNRT, 243 VALIANT trial, 85 Valsartan dosage, 209t elimination, 209t Valve sparing procedures, 437 Valvular disease, acute coronary syndromes, myocarditis and peripartum/postpartum cardiomyopathy (VAMP), 102 Valvular heart disease evaluation, 431 heart surgery, 431 HFrEF, 110 pathophysiology, 431 percutaneous intervention, 431–432 signs and symptoms, 431 Vancomycin, 71 Varenicline, 688–689 Vascular function, 718 Vascular site hemostasis, 58–59 Vascular ultrasound, 620–621, 621f Vasoconstrictors, 194 Vasodilator Heart Failure Trial (V-HeFT), 210 Vasodilators intestinal ischemia, 533 nesiritide, 207 nitroglycerin, 207 nitroprusside, 207 Vasoplegia, 194 Vasopressin, 323 Vasopressors acute heart failure, 104 pulmonary embolism, 484 Vasovagal syncope, 292 Venoarterial extracorporeal membrane oxygenation (VA-ECMO), 143, 144, 186 Venous thromboembolism (VTE) deep vein thrombosis See Deep vein thrombosis incidence, 477 new oral anticoagulants, 91 pathogenesis, 477 pulmonary embolism See Pulmonary embolism Veno-venous extracorporeal membrane oxygenation (VV-ECMO), 186 Ventilator-associated pneumonia (VAP), 473 Ventricular arrhythmia (VA) abnormal automaticity, 273 after STEMI, 18 antiarrhythmic medications, 283 basic definitions, 273, 274t, 283 cardiac magnetic resonance hypertrophic cardiomyopathy, 171–173 ischemic cardiomyopathy, 170–171 nonischemic cardiomyopathy, 171 causes, 283 durable left ventricular assist device, 188–189 heart transplantation, 195 and myocardial scarring, 133 nonsustained ventricular tachycardia, 273 obstructive sleep apnea, 216 premature ventricular complexes, 273, 274f reentry, 273 symptoms, 283 triggered activity, 273 types, 283 ventricular fibrillation, 278 ventricular tachycardia See Ventricular tachycardia Ventricular assist device (VAD) cardiogenic shock, 144 heart failure, 460 HFrEF, 113 Ventricular fibrillation (VF), 278, 284 Ventricular intrinsic preference (VIP), 302 Ventricular pace suppression (VPS), 302 Ventricular septal defect (VSD), 167, 453, 453f Ventricular septal rupture (VSR) clinical presentation, 126 incidence, 126 pathophysiology, 126, 126f treatment, 126–127, 127f, 128f Ventricular tachycardia (VT) adult congenital heart disease, 458–459 arrhythmogenic right ventricular cardiomyopathy, 280 atrioventricular dissociation, 275, 276f Brugada syndrome, 280 cardiac sarcoidosis, 281 catecholaminergic polymorphic, 280 catheter ablation, 284 commotio cordis, 281 dilated cardiomyopathy, 279–280 drug-induced, 281 fascicular, 279 focal, 279 hypertrophic cardiomyopathy, 280 ischemic heart disease, 279 long QT syndrome, 280 mitral valve prolapse, 281 pacing and electric shock, 284 pulseless sustained, 275 supraventricular tachycardia vs., 275, 275t sustained monomorphic, 276, 277f, 277t sustained polymorphic, 276, 278, 278f tetralogy of Fallot, 281 types and etiologies, 275, 275t Ventriculophasic sinus arrhythmia, 227 Verapamil acute decompensated HCM, 156 antiarrhythmic drug therapy, 340 nonobstructive HCM, 154 obstructive HCM, 154 Vernakalant, 339–340 Virchow triad, 477 Visual Analog Scale (VAS), 488 Vital exhaustion, 734 Vitamin K antagonists (VKAs), 351, 354t, 355–356 deep vein thrombosis, 483 intracranial hemorrhage, 525, 526t VO2 max, 724 Volutrauma, 469 VSR See Ventricular septal rupture VT See Ventricular tachycardia VTE See Venous thromboembolism VV-ECMO See Veno-venous extracorporeal membrane oxygenation W Wall Motion Score Index (WMSI), 32 Warfarin acute coronary syndrome, 91, 97 availability, 483t intracranial hemorrhage, 525, 526t modern anticoagulation therapy, 345, 354t, 355–356 Watchman LAA closure, 256, 257f Weaning, mechanical ventilator, 473 Weight loss and weight management, 715 Wells score, 480–481, 480t Wet signs, 100 White blood cell (WBC), 683 Wilkins Score/Mitral Valvuloplasty Score, 400t Windsock shape, LAA morphology, 256f Winged peripheral IV catheter system, 541f Wisconsin Sleep Cohort, 216 WiSE-CRT system, 303, 304f Women’s heart disease See Coronary microvascular dysfunction Women’s Ischemia Syndrome Evaluation, 694 ... rupture in fatally injured front-seat passengers in frontal car collisions: an autopsy study Am J Forensic Med Pathol 20 06 ;27 :29 2 -29 5 29 Smith RS, Chang FC Traumatic rupture of the aorta: still a lethal injury Am J Surg 1986;1 52: 660-663 Patient and Family Information for:... 1958;37 :21 7 -27 9 21 Eggebrecht H, Plicht B, Kahlert P, Erbel R Intramural hematoma and penetrating ulcers: indications to endovascular treatment Eur J Vasc Endovasc Surg 20 09;38:659-665 22 Stanson... Semin Thorac Cardiovasc Surg 20 14 ;26 : 123 -131 Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K Clinical features and long-term outcome of type A and type B intramural hematoma of the aorta J Thorac Cardiovasc Surg 20 04; 127 : 421 - 427