S3 vessels

Rupture

• -Elective – 5.0 - 5.5 cm diameter
• -Emergency – Rupture or impending rupture

• -Open
• -Endovascular

• 8x more common in men
• 50% have popliteal or femoral aneurysm
• 20% first oreder relatives with aneurysm

• 50% die before reaching hospital
• 25% of those reaching hospital alive, die before surgery
• 50% of those who undergo surgery survive
• 80% mortality overall

Popliteal aneurysm

Distal embolization and thrombosis

• Elective: > 2 cm diameter in relatively healthy patient
• Emergency: acute ischemia (thrombosis)

• -Splenic
• -Renal
• -Hepatic

• -Indications for Intervention
• Elective-- size > 2 cm (Usually found incidentally by CT)
• Emergency-- Rupture (usually splenic)
• Hypertension from compression of renal aneurysm on renal artery

• Most common visceral artery aneurysm
• Third most common intra-abdominal aneurysm
• Appear and are likely to rupture in multiparous women
• 4:1 female-to-male ratio
• Majority are calcified and all are saccular

• Most asymptomatic and are picked up incidentally
• LUQ discomfort
• “Double rupture phenomenon”
• Free rupture

• -Size > 2cm
• -Symptoms/signs of rupture or impending rupture

• -Surgical ligation/exclusion
• -Splenectomy for distal location
• -Trans-catheter embolization

• Male
• 60’s – 70’s
• Increased BP

• Chest Pain
• Anterior (Type A)
• Posterior (Type B)
• A,B - Stanford; 1,2,3 - Debakey

• Rupture
• -Pericardial tamponade
• -Hemomediastinum
• -Hemothorax (usually left-sided)
• Occlusion of Aortic Branch Vessels
• -Carotid (stroke)
• -Coronary (myocardial infarction)
• -Splanchnic (organ infarction)
• -Renal (acute renal failure)
• -Iliac, brachiocephalic, subclavian (limb ischemia)
• Distortion of Aortic Annulus
• -Aortic regurgitation

• Type A
• -Surgery

• Type B
• -Medical (decrease BP)
• -Intervention for branch complications (open/endovascular)

• Patency of false lumen is a risk factor for progression of chronic dissection to aneurysmal dilatation
• Induce false lumen thrombosis by sealing the aortic tear with an aortic endograft
• Redirects flow into the true lumen
• Treats malperfusion syndromes caused by dynamic obstruction and minimizes aneurysmal degeneration of the outer wall of FL

• Thrombotic (atherosclerotic--PVD)
• Embolic
• Macroembolic (heart)
• Microembolic (proximal artery)
• Vasculitis

• =CAD
• Same risk factors
• 40% of PVD patients have CAD

• Smoking
• Diabetes mellitus
• Genetics
• Hypertension
• Hyperlipidemia
• Radiation

• Lower extremity arteries
• Carotid arteries
• Visceral arteries
• -Renal
• -Mesenteric

Femoral bifurcation 40%

• Cardiogenic 80%
• -Atrial Fibrillation 50%
• -Myocardial 25%
• 10% noncardiac
• 10% idiopathic

• Feet/toes (“blue toe” syndrome)
• Hands/finger tips
• Brain

• Thrombotic (PVD) or embolic
• Sudden complete occlusion of artery
• Common to all: PAIN

• Low ankle-brachial index
• 5 P’s
• -Pallor
• -Pulseless
• -Paralysis
• -Pain
• -Paresthesias

• Thrombotic (PVD)– long-standing
• Legs
• -Claudication
• -Rest pain
• -Tissue loss
• Bowel
• -Post-prandial pain
• Kidney
• -Hypertension
• -Loss of parenchyma

• Embolectomy
• Treat underlying heart problem
• Anticoagulation

• Open Surgery
• -Bypass
• -Endarterectomy
• Endovascular
• -Angioplasty
• -Atherectomy
• -Stent

• Hemispheric TIA or amaurosis fugax with a > 70% stenosis
• Completed stroke with an excellent recovery and a > 70% stenosis
• Asymptomatic stenosis of > 80% in a “good risk” patient

• Treatment of HTN is the most common reason for office visits of non-pregnant adults to physicians in the United States and for use of prescription drugs
• Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
• Prehypertension: systolic 120-139 mmHg or diastolic 80-89 mmHg
• Hypertension:
• --Stage 1: systolic 140-159 mmHg or diastolic 90-99 mmHg
• --Stage 2: systolic ≥160 or diastolic ≥100 mmHg

• Alcohol
• Aortic coarctation
• Renal disease
• Renal artery stenosis
• Pheochromocytoma
• Primary aldosteronism
• Cushing’s syndrome
• Sleep apnea
• Thyroid dysfunction
• Hypercalcemia
• Drugs
• -Oral contraceptives
• -NSAID’s
• -Cocaine

• Acute, life threatening episodes of severe HTN with end organ damage (CNS, CVS, renal)
• Most commonly in patients with h/o uncontrolled HTN, non compliance
• BP usually >180/120

• Cerebral infarction
• Pulmonary edema, CHF
• Encephalopathy
• ICH
• Aortic dissection
• Eclampsia

• Severe HTN without end organ damage or symptoms, other than headache
• BP usually >180/120
• Most commonly in patients with h/o uncontrolled HTN, non compliance

Direct Cardiac: Congestive heart failure, Ischemic heart disease, Atrial fibrillation

Non Cardiac: Cerebrovascular, Renal

After age 40, the lifetime risk of developing CHF was 2X as high in subjects with a blood pressure ≥160/100 mmHg compared to <140/90 mmHg

HTN directly leads to left ventricular hypertrophy

Hypertensive heart disease

• Immobility
• Increasing age
• Surgery (pelvic)
• Trauma
• Malignancy
• Pregnancy
• Central venous catheters
• Hyperhomocystinemia
• Estrogenic meds (BCP)
• Inherited thrombophilias
• Increased blood viscosity (Sickle cell, polycythemia, Multiple Myeloma etc)

• Abnormal pulmonary gas exchange
• Pulmonary hypertension
• Right ventricular failure
• Cardiogenic Shock
• Atelectasis

• Acute unexplained dyspnea
• Pulmonary hemorrhage/infarction
• Acute cor pulmonale / cardiogenic shock / syncope / sudden death
• S/S of DVT – unilateral thigh or calf engorgement

• Arterial hypoxemia / respiratory alkalosis
• Dyspnea / hypoxemia not responsive to bronchodilator therapy
• Fever
• Unexplained atelectasis or pleural based infiltrate
• Sudden increase in pulmonary pressures
• Sudden increase in CVP and decresed organ perfusion
• Unexplained tachypnea / tachycardia

• CXR – rarely helpful, can point to other diagnoses (# rib, CHF, pneumonia)
• ECG – classic – deep S in I, Q in lead III, inverted t in lead III (S1Q3T3)
• D- Dimer – negative predictive value better than positive
• Imaging: V/Q scan, CT angiography, pulmonary angiography

• negative D-Dimer in setting of pre-test low or moderate probability rules out PE
• High rate of false positives

• Mismatched V/Q abnormalities
• -A normal scan within days of event reliably rules out PE
• -A perfectly unmatched defect is highly suggestive (>90%) of PE
• Matched abnormalities
• -indeterminate

• Unlikely -> dimer -> negative no
• Positive dimer or likely PE -> Chest CTA/V/Q scan --> positive treat, negative no
• Equivocal--> Ultrasoudn DVT, consider angiogram

Both: Chest pain, shock, dyspnea

In Massive PE: RV heave, Incr P2, Rt S3, neck vein distension, clear lungs

In AMI: No heave, muffled heart sounds, S3 and S4, crackles (pulmonary edema)

• Anticoagulate
• Increase Preload (fluid)
• CPR * compressions can dislodge or disrupt clot
• Inotropic support
• Consider thrombolytic therapy (rTPA)
• Mechanical strategies

• IVC filter
• Recurrence despite anticoagulation
• When anticoagulation is contraindicated
• Patients with PE at high mortality risk if recurrent
• Surgical or catheter embolectomy
• Limited utility – patients are unstable and sick
• Most improve by the time it is considered

• Deep venous thrombosis (DVT)
• Valvular incompetence (reflux) - trauma, dilation with age, thrombus causes scar

• Pain
• Edema
• Erythema
• Tenderness
• Fever
• Prominent superficial veins
• Pain with passive dorsiflextion of foot (Homans’ sign)
• Peripheral cyanosis
• Massive pitting edema and blanching (phlegmasia cerulea albans)
• Painful blue leg (phlegmasia cerulea dolens)

• Lab: D-dimer
• Imaging:
• -Duplex ultrasound
• -Venography
• -Magnetic resonance venography
• -Computed tomographic venography

• Anticoagulation
• Inferior vena cava (IVC) filter if anticoagulation contraindicated
• Thrombolysis with tissue plasminogen activator (tPA) if DVT is severe and disabling in young patient
• Compression therapy (elastic stockings) to prevent long-term skin complications of chronic venous insufficiency

• Pulmonary embolism
• Pulmonary hypertension after PE
• Death from PE
• Post-thrombotic syndrome (chronic venous insufficiency - varicose veins, edena, skin changes, ulceration)

• ST with varicose veins
• Traumatic
• Septic/suppurative
• Migratory thrombophlebitis (Trousseau’s syndrome)
• SSV thrombophlebitis
• Upper extremity

• Antibiotics
• NSAIDs
• Warm compresses
• Anticoagulation
• Limb elevation

Thrombosis, inflammation, and possibly infection of a superficial vein

Signs/symptoms: Erythema, Tenderness, Palpable cord

• Venous congestion of head and neck secondary to central venous obstruction
• Signs/Symptoms – facial swelling, plethora, cough, dyspnea, stridor

• Intraluminal fibrosis - benign (TB, hypercoaguable, syphilis, defib, pacemaker, catheter
• or
• External compression - 80% malignant, also benign

Stent placement

• Lymphedema
• Interstitial accumulation of lymph due to impaired drainage

• •Classification of lymphedema based on etiology, age of onset, and
• inheritance

• •Primary lymphedema
• –Congenital (onset less than 1 year of age)
• •Nonfamilial
• •Familial (Milroy’s disease)
• –Lymphedema praecox (onset from 1-35 years of age)
• •Nonfamilial
• •Familial (Meige’s disease)
• –Lymphedema tarda (onset after 35 years of age)
• •Secondary lymphedema
• –Filariasis
• –Lymph node excision/radiation
• –Tumor invasion
• –Infection
• –Trauma

• •Signs/symptoms
• –Edema
• –Skin changes
• •Peau d’orange
• •Lichenification
• •Ulcerations rare (unlike venous stasis)
• •Complications
• –Infection (lymphangiitis)
• –Malnutrition
• –Immunodeficiency
• –Malignancy (Stewart-Treves)
• •Treatment
• –Sequential mechanical compression

Smoking

non-Hispanic blacks

• •HsCRP adds prognostic information at all levels of LDL cholesterol and at all levels of risk, as determined by the Framingham Risk Score
• •In clinical terms, absolute vascular risk is higher in individuals with elevated hsCRP levels and low levels of LDL cholesterol than in those with elevated LDL cholesterol but low levels of hsCRP

• marker of inflammation
• Hiperhomocysteinemia patients present with endothelial dysfunction, accelerated oxidation of LDL cholesterol, impairment of flow-mediated endothelium-derived relaxing factor with subsequent reduction in arterial vasodilation, platelet activation and oxidative stress

• Impaired fibrinolysis can result from an imbalance between the clot dissolving enzymes t-PA or urokinase-type plasminogen activator and their endogenous inhibitors, primarily PAI-1
• A consistent series of prospective studies has linked abnormalities of fibrinolysis to increased risk of arterial thrombosis

The close homology between Lp(a) and plasminogen has raised the possibility that this lipoprotein may inhibit endogenous fibrinolysis by competing with plasminogen binding on the endothelium

• Same as angina: Retrosternal chest pressure, burning or heaviness; radiating occasionally to neck, jaw, epigastrium, shoulders, or left arm.
• Sudden onset, usually lasting 30 minutes or longer. Often associated with shortness of breath, weakness, nausea and vomiting.

• Sharp, pleuritic pain aggravated by changes in position; highly variable duration
• Pericardial friction rub

• Sudden onset of dyspnea and pain, usually pleuritic with pulmonary infarction
• Dyspnea, tachypnea, tachycardia, and signs of right heart failure

• Substernal chest pressure, exacerbated by exertion.
• Pain associated with dyspnea and signs of pulmonary hypertension.

• Burning discomfort in midline with dyspnea.
• Abrupt onset of dyspnea and pain.

• Pleuritic pain, usually brief, over involved area.
• Pain pleuritic and lateral to midline, associated with dyspnea.

• 4 to 8 hours after the onset of STEMI
• declines to normal within day 2 or 3

• •Released from injured myocardial cells
• •Peak levels are reached 1 to 4 hours after the onset of MI
• •Poorly specific
• •Should be supplemented by troponins (cTnI or cTnT)

• Start to rise by 3 hours after the onset of chest pain
• Elevations of cTnI may persist for 7 to 10 days after MI
• Elevations of cTnT may persist for up to 10 to 14 days
• Very useful for late diagnosis of MI

The definition of acute coronary syndrome (ACS) includes unstable angina (UA), non-ST segment elevation myocardial infarction (non-STEMI), and ST segment myocardial infarction (STEMI). However, in practice, ACS is used to indicate UA and non-STEMI

• ACS is result of a mismatch between myocardial oxygen supply and demand
• Occasionally, this is due to anemia, hyperthyroidism, infection, tachyarrhythmias, or valvular heart disease
• MOST COMMON CAUSE of change from stable CAD to ACS is disruption or fissuring of a vulnerable atherosclerotic plaque; this is followed by platelet-mediated thrombosis and vasoconstriction with or without elevation of cardiac markers

coronary atherosclerosis, with thrombosis

• Plaques prone to disruption overexpress metalloproteinase enzymes
• Plaque disruption can be produced by stresses induced by intraluminal pressure, coronary vasomotor tone, tachycardia and disruption of nutrient vessels
• BP, HR, blood viscosity, t-PA, PAI-1, cortisol and epinephrine in high levels may cause plaque disruption

• •Coronary embolism: endocarditis, mural thrombi, prosthetic valves, neoplasms
• •Inflammatory processes:
• •Infections- viral (Echo, Coxsackie), syphilitic aortitis
• •Takayasu arteritis
• •Necrotizing arteritis
• •Polyarteritis nodosa
• •Kawasaki disease

• •SLE
• •Radiation
• •Amyloidosis
• •Hurler syndrome
• •Homocystinuria
• •Cocaine abuse

• Rales audible in patients with LV failure
• Diffuse wheezing can be present in patients with severe LV dysfunction
• Cough with hemoptysis suggesting pulmonary embolism with infarction can also occur

• First sound frequently muffled and occasionally inaudible after the infarct
• Patients with marked ventricular dysfunction and/LBBB may have splitting of S2
• S4 almost universally present in patients with STEMI, limited diagnostic value, S3 reflects severe LV dysfunction

• •Systolic murmurs are commonly audible, generally result from MR secondary to papillary muscle dysfunction
• •An apical holosystolic murmur with a thrill may represent rupture of papillary muscle
• •In the rupture of the IV septum are similar but murmur and thrill are more prominent in the left sternal border
• •The systolic murmur of tricuspid regurgitation is also heard along the left sternal border (intensified by inspiration)

• May be heard in patients with STEMI
• Probably more common than reported
• Most commonly noted on second to third day after MI
• In patients with STEMI and friction rub may have a pericardial effusion
• Dressler syndrome: Post-infarction pericarditis (up to 3 months after MI)

• History of ischemic-type chest discomfort
• Evolutionary changes on serial ECG traces
• Rise and fall in serum cardiac markers