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Cardiology > Gender issues in CVD > Flashcards

Gender issues in CVD Flashcards

1
Q

Since 1984, more ______ than _____ die from CVD

A

-women than men

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2
Q

Younger men may have a greater incidence of CV events, but more women ______.

A
  • die
  • post-MI mortality is higher in younger women
  • men get first event soon that women in all age groups, but more women die
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3
Q

__________ have less obstructive coronary artery disease at angiography in ACS.

A

-women

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4
Q

Women have more pathophysiology in men in what 6 categories?

A
  • focal atherosclerosis
  • diffuse atherosclerosis
  • coronary vasospasm
  • endothelial dysfunction
  • small vessel disease
  • spontanteous coronary artery dissection
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5
Q

CV deaths affect predominantly women over the age of _____.

A
  • 65

- due to potential premenopausal cardioprotective effects

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6
Q

Positive effects of estrogen on the CV system

A
  • decrease LDL, increase HDL
  • facilitates NO vasodilation
  • inhibits detrimental response of blood vessels to injury and development of atherosclerosis
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7
Q

Negative effects of estrogen on CV system

A
  • increasing TGs
  • increases inflam. marks like CRP
  • prothrombotic effects: increase prothrombin and decrease antithrombin III–DVTs
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8
Q

Framington investigators reported a ______ fold higher incidence of CV events in post vs premenopausal women. Does HRT work?

A
  • 2.6 fold

- HRT controversial; increased risk for breast cancer and not seen to be effective for establish atherosclerosis

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9
Q

Testosterone subfractions

A
  • most not bioavailable as boudn to SHBG

- rest is weakly bound to albumin or free T

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10
Q

T/F: Testosterone deficiency in men may lead to increased CV risk

A
  • true
  • T deficiency: increasing inflammation, increased coronary intima-media thickness, worsens metabolic syndrome
  • *conflicting data
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11
Q

5 Effects of T on CVS

A
  • causes vasodilation independent of NOS
  • may reduce angina threshold: improves exercise tolerance
  • shorten QT interval
  • reduced in pts with CHF
  • increases exercise tolerance in CHF without effecting LVEF
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12
Q

T replacement therapy

A
  • also controversial

- seen to increase DVT and PE risk, BPH and Prostate cancer, and increase hematocrit

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13
Q

Why are pregnant women often anemic?

A

-increase in plasma volume (by 50%) more so than increase in RBC, though both increase in pregnancy

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14
Q

Physiologic changes in pregnancy concerning CO, SV, HR, and TPVR

A
  • increase CO, SV, and HR, increase blood vlume
  • decrease TPVR, maybe dec BP
  • decrease pulm VR
  • increase venous P in lower extremities
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15
Q

What causes the increased venous P in lower extremities of pregnant women?

A

-fetus pushing on IVC

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16
Q

Hemodynamic changes of labor and delivery

A
  • each uterine contraction= 500 ml blood released into circ to rapid increase CO and BP
  • delivery blood loss is 400 ml or 800 with c-section
  • after delivery, abrupt increase in venous return
17
Q

What accounts fro abrupt increase in venous return to mom after delivery?

A
  • autotransfusion from uterus: continues in 24-72 hrs after delivery–Pulm edema if CHF or valve issues
  • baby no longer compresses IVC
18
Q

high risk pregnancies mom profiles

A
  • pulm HTN
  • dilated CM, ej <40%
  • symptomatic obstructive lesions (cannot change CO needed in preg): AS, MS, pulm stenosis, coarctation of aorta
  • cyanotic lesions
  • mechanical prosthetic valves
19
Q

Pulmonary HTN is most commonly caused in childbearing years by what?

A

-secondary to a shunt in setting o VSD, PDA, or ASD

20
Q

Regardless of the cause, pulmonary HTN carried very high mortality in pregnancy. Give stats for severe pulm HTN in Eisenmenger syndrome-

A

maternal mortality ~50% and perinatal mortality may exceed 25%

21
Q

Current recommendations for pts with severe PHTN

A

-termination of pregnancy if it occurs

22
Q

Issues with PHTN and pregnancy

A
  • V load of pregnancy may compromise poorly functioning RV leading to heart failure
  • if shunt exists, fall in PVR augments right-to-left shunting and may worse cyanosis
23
Q

Stenotic lesions induce ______ overloaded state, with fixed valve orifices that limit heart’s ability to augment _____.

A
  • pressure

- CO

24
Q

How does MS cause exertional pulmonary edema?

A
  • when MV orifice area is sufficiently reduced, blood moves from LA to LV onky if propelled by pressure gradient
  • elevated LA P raises pulmonary venous and cap pressures
25
Q

MS in pregnancy

A

Increased blood flow across MV results in further elevation of the LA pressure
Increased heart rate results in decreased diastolic filling time, resulting in reduction in forward cardiac output
Atrial fibrillation can cause further decompensation (increased heart rate and loss of atrial contraction
Patients at highest risk for decompensation are those with moderate to severe MS and cardiac events prior to pregnancy

26
Q

How to manage MS in pregnancy

A

Beta blockade, judicious use of diuretics, bed rest can be useful in the medical management of symptomatic patients.
Women with severe MS should be considered for percutaneous balloon valvotomy before conception, if possible.
Percutaneous balloon valvotomy is a reasonable option for women who develop severe symptoms during pregnancy

27
Q

Are stenotic or regurgitant lesions better tolerated in pregnancy?

A

-Regurgitant lesions, which impose volume overload on the heart, tend to be better tolerated than stenotic lesions as patients can still accommodate increased flow and cardiac output required in pregnancy

28
Q

Cyanotic Heart Disease

A

Decrease in peripheral resistance in pregnancy augments the right-to-left shunt and may exaggerate maternal cyanosis
Erythrocytosis that accompanies cyanosis increases propensity for thrombosis, and thus the risk of paradoxical embolism and stroke
Maternal hypoxia impedes fetal growth and survival

29
Q

Pregnancy for women with prosthetic valve poses risk to _________.

A

-both mother and fetus

30
Q

Tissue vs mechanical valve for women considering pregnancy

A
  • tissue advantage: less thrombogenic, does not need warfarin, disadvantage: degenerates within 10 years, so need reoperation
  • mechanical advantage: greater longevity, disadvantage: thrombogenic, needs warfarin
31
Q

Anticoagulation therapy in pregnancy

A

Management of anticoagulation in pregnancy when mother has mechanical valve is controversial
Each potential modality is associated with greater risks to both mother and fetus.Risks to mother: Higher incidence of valve thrombosis/embolic phenomenon due to Increased concentration of clotting factors in pregnancy and Increased platelet adhesiveness, decreased fibrinolysis
Risks to fetus: Higher incidence of fetal loss, placental hemorrhage. Possible embryopathy with warfarin.

32
Q

Fetal exposure to warfarin

A
  • exposure in 1st trimester is associated with fetal embryopathy, and may also increase risk of fetal loss/abortion
  • embryopathy may be dose related, so low doses </ 5 mg has low incidence
33
Q

Unfractionated Heparin in pregnancy

A
  • large mlc that does not cross placenta so no developmental abnormalities in fetus
  • SQ or IV
  • often started when preg dx and continued past 1st trimester when warfarin is resumed
  • hep resumed week 35 since shorter acting in case of delivery
34
Q

Peripartum CM

A

-Dilated cardiomyopathy with LV dysfunction occurring in last month of pregnancy or within 5 months of delivery
-1 in 3000
-Most patients (~75%) present with symptoms in first month post-partum (?autoimmune ?)
Normalization of function is noted in ~50% of cases (more likely if LVEF >30% at diagnosis)

35
Q

Peripartum CM risk factors

A

Risk factors include multiparity, older maternal age, preeclampia, black ethnicity

36
Q

Should women with peripartum CM worry about future pregnancies?

A

-yes, recur in up to 30% of cases–warn against getting knocked up again

37
Q

Rx of peripartum cardiomyopathy

A

Treatment is the same as other forms of cardiomyopathy, with the caveat that ACE-I and ARB cannot be used during pregnancy

Cardiology (27 decks)

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