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CARDIOVASCULAR DISEASES IN PREGNANCY

Joanna Zerline Lozada-Pascual, MD, FPOGS, FPSMFM

Department of OB-GYN

12 July 2011

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Heart Disease

Leading cause of death in women who are 25-44 yrs old

Cardiovascular physiology

Increase in blood volume by 40 to 60% starting early in first trimester, mainly due to expansion of plasma volume

Cardiac output increases by 40 to 50% beginning in first trimester, with peak at the 20-24th week, initially due to SV increase, later due to HR increase

Peripheral vascular resistance decreases during pregnancy causing a decrease in diastolic blood pressure, especially in the early trimester

Increase in heart size due to eccentric hypertrophy

BP declines in mid-pregnancy due to decreased total peripheral resistance and the rise in cardiac output.

*Patients who fail to exhibit a drop in BP are more likely to develop preeclampsia.

During labor : 500 ml of blood is “autotransfused” into maternal circulation resulting in increased BP and cardiac output.

Peaks of Cardiac Activity during Pregnancy

These are during the early third trimester, during labor, during delivery and during the puerperium.

Changes in Diagnostic Tests Findings during Pregnancy

normal pregnancy,

functional systolic heart murmurs are common; respiratory effort is accentuated and at times suggests dyspnea; edema in the lower extremities after midpregnancy is common; and fatigue and exercise intolerance develop in most women

1. Cardiac Physical Examination

Increase in the intensity of first heart sound with exaggerated splitting

May have systolic ejection flow murmurs

Diastolic murmurs are rare and would warrant further study

2. Chest X-ray Film

Lordosis can create straightening of the left upper cardiac border, mimicking left atrial enlargement

Elevation of the diaphragm causes more horizontal position of the heart

Pulmonary vasculature appears more prominent

3. Electro-cardiogram

Horizontal position of the heart causes left or right shift of QRS

Transient ST-segment an t-wave changes are common

Right axis deviation, RBBB, or ST depression of 1 mm on left precordial leads

Q waves in lead III, T wave inversion in III, V2 and V3

Small decreases of PR and QT

Rotation of =/- of 15 degrees (QRS axis)

Atrial and ventricular premature contractions are relatively frequent

Pregnancy does not alter voltage findings

4. Echocardiogram

allows noninvasive evaluation of structural and functional cardiac factors

Increase in end-diastolic and end-systolic ventricular measurements with no increase in wall thickness

Mild tricuspid regurgitation may be due to increase volume

Increased Trivial tricuspid regurgitation (43 to 94% at term)

Pulmonary regurgitation (94% at term)

Increased left atrial size by 12 to 14%

Increased LV end diastolic dimensions by 6-10%

Inconsistent increase in LV thickness / left ventricular mass

Pericardial effusions

5. Pulmonary artery catheterization – no change

Clinical Findings of HD

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SYMPTOMS

Severe or progressive dyspnea

Nocturnal cough

Hemoptysis

Syncope with exertion

Chest pain related to effort or exertion

CLINICAL FINDINGS

Cyanosis

Clubbing of the fingers

Persistent neck vein engorgement

Systolic murmur greater than Gr III/VI

Diastolic murmur

Cardiomegaly

Sustained arrhythmia

Persistently split S2

Loud P2 (criteria for pulmonary hypertension)

New York Heart Association Classification

Class I Uncompromised, with no limitation of cardiac activity. No symptoms of cardiac insufficiency or anginal pain.

These patients usually go through pregnancy well . But should still watch out for any complication which may push them into failure.

Management

Avoid contact with persons who have respiratory infections

Pneumococcal and influenza vaccines

Cigarette smoking is prohibited

NSD preferred

During labor, kept in semirecumbent position with lateral tilt

Epidural analgesia for NSD minimize intrapartum CO fluctuations and allows forceps or vacuum assited delivery

CS: epidural anesthesia

SE conduction analgesia: maternal hypotension

Tubal sterilization and contraception best after vaginal delivery and woman is stable, afebrile, not anemic, ambuates normally

Class II Slightly compromised, with slight limitation of physical activity. Comfortable at rest, but with ordinary or usual physical activity, the patient experiences excessive fatigue, palpitation, dyspnea or anginal pain.

Management is the same as that for Class I, but more vigilance in watching out for complications is made because of the higher incidence of complications.

Class III

Markedly compromised, with marked limitation of physical activity.Comfortable at rest but symptomatic with less than ordinary activity.

These patients must be co-managed with an internist-

Management

Impt question whether pregnancy should be undertaken

If women make that choice, they must understand the risks and cooperate fully with planned care.

cardiologist. These patients may have to be admitted, as one-third of them will decompensate to class IV. Labor must be in the hospital. Counseling on the risk of pregnancy must be made.

If feasible, women with some types of severe cardiac disease should consider pregnancy interruption.

If the pregnancy is continued, prolonged hospitalization or bed rest is often necessary.

Anesthesia: epidural

NSD preferred

Class IV

Severely compromised. Unable to perform any physical activity without discomfort. Symptoms are present at rest and are increased with any physical activity.

Treat the decompensation, and then manage any obstetric problem. This is associated with high maternal mortality rate. Close coordination with the cardiologist is made. Counseling on the risk of pregnancy is made.

Predicting Cardiac Complications during Pregnancy

Prior heart failure, transient ischemic attack, arrhythmia, or stroke

Baseline NYHA Class III or greater or cyanosis

Left-sided heart obstruction defined as mitral valve area below 2 cm2, aortic valve area below 1.5 cm2, or peak ventricular outflow tract gradient above 30 mm Hg by echocardiography

Ejection fraction less than 40%

most important predictors of complications were prior congestive heart failure, depressed ejection fraction, and smoking

(William’s Obstetrics 23rd edition, 2010)

Signs and Symptoms of Congestive Heart Failure

persistent rales at the lung bases – first warning sign of CHF

sudden diminution of the capacity to work

increasing dyspnea on exertion

hemoptysis (usually associated with pulmonary hypertension)

progressive dyspnea, edema and tachycardia

Presence of any of these symptoms warrants admission. Much of the load on patients occurs at around the second half of pregnancy

Table 2: ACOG Classification of Risks for Maternal Mortality Caused by Various Types of Heart Disease

Group 1 Minimal Risk

Atrial septal defect

Ventricular septal defect

Patent ductus arteriosus

Pulmonic or tricuspid disease

Corrected tetralogy of fallot

Bioprosthetic valve

Mitral stenosis, NYHA Class I and II

0-1 %

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Group 2A Moderate Risk

Mitral stenosis, NYHA class III and IV

Aortic stenosis

Aortic coartation without valvular involvement

Fallot tetralogy, uncorrected

Previous myocardial infarction

Marfan syndrome, normal aorta

5-15%

Group 2B Moderate Risk

Mitral stenosis with atrial fibrillation

Artificial valve

5-15%

Group 3 Major Risk

Pulmonary hypertension

Aortic coarctation with valvular involvement

Marfan syndrome with aortic involvement

25-50%

Mitral Stenosis

Rheumatoid endocarditis – causes ¾ of mitral stenosis

Contracted valve impedes blood flow from the left atrium to the right ventricle

8% develop congestion,

6 % experience symptomatic atrial arrhythmia

1-2% may have embolism.

About less than half develop pulmonary hypertension, which is a poor prognostic factor

Indications for surgical treatment:

1. Non-responsive pulmonary edema

2. History of pulmonary edema, even with good medical treatment

3. Profuse and profound hemoptysis

Most common RHD in pregnant patients

Primary symptom : Easy fatigability

Patients (ideally) should undergo surgical correction prior to pregnancy

Features :

fixed CO ,

shortened diastolic filling time,

elevated left atrial and

pulmonary capillary pressure

Management

Limit activity + diuretic therapy + dietary sodium restricted

(+) atrial enlargement : anticoagulation is indicated

Valvuloplasty or valve replacement may be necessary if medical therapy fails

During Labor and Delivery :

invasive hemodynamic monitoring may be helpful

Epidural anesthesia, control of HR , supplemental O2 , semi-fowler’s positioning , avoidance of Valsalva , and assisted forceps delivery are advisable.

Puerperium : most hazardous time

May need diuretics to prevent pulmonary edema Aortic Stenosis

disease of aging, and in women younger than 30 years, it is most likely due to a congenital lesion

Uncommon during pregnancy

Stenosis reduces the normal 2- to 3-cm2 aortic orifice and creates resistance to ejection

Features :

1. Fixed Stroke Volume assoc with stenosis

Exertion may result to dec. O2 delivery to the cerebral and coronary vessels

2. LV Hypertrophy : compensatory

increases O2 needs of the myocardium

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Pregnancy is contraindicated if valve area is < 1cm2

(+) Angina , dyspnea , and syncope :

5 yr mortality rate ~ 50% Management

asymptomatic woman with aortic stenosis, no treatment except close observation is required

strict limitation of activity and prompt treatment of infections

key to mgt: avoidance of decreased ventricular preload and maintenance of CO

during L&D: managed on the “wet” side maintaining a margin of safety in intravascular volume in anticipation of possible hemorrage

Avoid tachycardia , maintain filling pressures , prevent decreased CO and pulmonary edema

Regional anesthesia : use with extreme caution

Valve replacement , valvulotomy , or balloon valvuloplasty may be necessary

Mitral Regurgitation/ Insufficiency

improper coaptation of mitral valve leaflets during systole, some

degree of mitral regurgitation develops followed by left ventricular dilatation and eccentric hypertrophy

Chronic mitral regurgitation causes

rheumatic fever,

mitral valve prolapse,

or left ventricular dilatation of any etiology—for example, dilated cardiomyopathy

Less common causes include a calcified mitral annulus, possibly some appetite suppressants, and in older women, ischemic heart disease

Mitral valve vegetations—Libman-Sacks endocarditis—common in women with antiphospholipid antibodies

• Acute mitral insufficiency caused by rupture of a chorda tendineae, infarction of papillary muscle, or leaflet perforation from infective endocarditis

Mitral valve prolapse. , Rheumatic fever , or aortic flow obstruction

Reduced ventricular output = fatigue and dyspnea

Atrial enlargement may lead to AF in long-standing cases

Goal of mgt : reduce LV afterload

Epidural anesthesia : recommended

Atrial Regurgitation/ Insufficiency

diastolic flow of blood from the aorta into the left ventricle

Causes: RF, connective-tissue abnormalities, congenital lesions

With Marfan Syndrome aortic root may dilate, resulting in regurgutation

Aortic and mitral valve insufficiency have been linked to the appetite suppressants fenfluramine and dexfenfluramine and to ergot-derived dopamine agonists

Rarely causes LV failure until the 4th or 5th decade of life

Complicates pregnancy in <10% of cases

Mgt Goals : reduction in afterload

restrict activity

(+) Heart failure : digoxin + diuretics

Epidural anesthesia : recommended

Bradycardia inc. regurgitation across the valve and is poorly tolerated.

Bacterial endocarditis prophylaxis may be recommended

Pulmonic Stenosis

usually congenital and also may be associated with Fallot tetralogy or Noonan syndrome

Noonan Syndome - autosomal dominant congenital disorderconsidered to be a type of dwarfism, that affects both males and females equally.

principal features include congenital heart defect (typically pulmonary valve stenosis), short stature, learning problems, pectus excavatum, impaired blood clotting, and a characteristic configuration of facial features including a webbed neck and a flat nose bridge

Dx: identified by auscultating a systolic ejection murmur over the pulmonary area that is louder during inspiration.

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Congenital Heart Disease

ASD - atrial septal defects, without pulmonary hypertension

VSD - ventricular septal defects, without pulmonary hypertension or left-to-right shunts

PDA - patent ductus arteriosus which was corrected in childhood. If it is not corrected, or if it is with a large left-to-right shunt, pregnancy can result in left ventricular overload and failure

Pulmonary and Tricuspid valvular lesions, unless, severely compromised predating pregnancy

Two most common congenital problems are VSD and ASD

Both are abnormal holes in the wall between the side of the heart that pumps oxygen-poor blood to the lungs, and the side that pumps oxygen-rich blood out to the body.

Complication occurs if with pulmonary hypertension

VENTRICULAR SEPTAL DEFECT (VSD)

Small VSDs : well tolerated

if the defect is less than 1.25 cm2, pulmonary hypertension and heart failure do not develop

(+) L to R shunting inc. pulmonary vascular resistance reverse shunting with cyanosis occurs

When pulmonary arterial pressures reach systemic levels, however, there is reversal or bidirectional flow—Eisenmenger syndrome (Eisenmenger syndrome)

Epidural anesthesia : may not be tolerated

During labor : if cyanosis develops = R to L shunting

Supplemental O2 + measures to inc. vascular resistance + invasive hemodynamic monitoring

ATRIAL SEPTAL DEFECTS (ASD) :

Common in adults

Most common form : Ostium secundum defect

asymptomatic until the third or fourth decade

Assoc. with mitral valve prolapse or regurgitation

R sided failure and arrhythmias : 4th or 5th decade of life

potential to shunt blood right to left makes possible a paradoxical embolism—entry of a venous thrombus through the septal defect and into the systemic circulation embolic stroke

Management:

During pregnancy : well tolerated and requires no specific therapy in most gravidas

Invasive monitoring : rarely needed

Epidural anesthesia : preferred

Compression stockings+prophylactic heparin in othe presence of immobility

Bacterial endocarditis prophylaxis

ATRIOVENTRICULAR SEPTAL DEFECT

characterized by a common, ovoid-shaped AV junction

associated with aneuploidy, Eisenmenger syndrome, and other malformations, some of these women become pregnant

PATENT DUCTUS ARTERIOSUS (PDA) :

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Shunts blood from high pressure aorta to the lower pressure pulmonary artery

Usually corrected during childhood

Small PDAs : well tolerated in pregnancy

Benign course until middle ages

TETRALOGY OF FALLOT (TOF) :

a. RV outflow obstruction

b. VSD

c. RV hypertrophy d. Aorta overriding the VSD

R to L shunting : usually present

Uncorrected lesions :

reduced life expectancy

Pregnancy is rare

If (+) pregnancy =spontaneous abortion , IUGR , cardiac failure

Corrected lesions :

Pregnancy : well tolerated

Inc. risk of IUGR

During Labor and Delivery :

Supplemental O2 + efforts to maintain venous return

Narcotics or pudendal block : vaginal delivery

General anesthesia : CS delivery

Vaginal delivery preferred

COARCTATION OF THE AORTA :

Usually corrected during infancy

Clinical : BP gradient between upper and lower extremity

Isolated HPN in the R upper arm

Fixed stroke volume

Cerebral berry aneurysms : common

Patients with prior repair should be reevaluated for aortic narrowing

DEVELOPMENTAL CARDIAC LESIONS

EISENMENGER’S SYNDROME :

secondary pulmonary hypertension that develops from any cardiac lesion

R to L shunt (via ASD , VSD , or PDA) underlying defects

elevated pulmonary vascular resistance

Maternal (12-70%) and fetal (50%) mortality are high

Cyanosis ,chest pain , syncope , and hemoptysis : poor prognosis

Termination of pregnancy is an option

For patients who continue with pregnancy : limit activity , anticoagulation , maintenance of preload , supplemental O2 , avoid hypovolemia

PULMONARY HYPERTENSION

N resting mean pulmonary artery pressure 12-16mmHg

a hemodynamic observation and not a diagnosis—is defined in nonpregnant individuals as a mean pulmonary pressure >25 mm Hg

Class I indicates a specific disease that affects pulmonary arterioles. It includes idiopathic or "primary" pulmonary hypertension as well as those cases secondary to a known cause such as connective-tissue disease

Class II disorders are more commonly encountered in pregnant women caused by left-sided atrial, ventricular or valvular disorders

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Clinical Classification of Some Causes of Pulmonary Hypertension in Pregnancy

I. Pulmonary arterial hypertension

Idiopathic – primary pulmonary HPN

Familial eg. Chromosome 2 gene in TGF superfamily

Assoc with: collagen vascular disease, congenital left-to-right shunts, HIV infection, thyrotoxicosis, sickle cell hemoglobinopathis, APAS, portal HPN

Persistent pulmonary HPN in newborn

other

II. Pulmonary hypertension with left-sided heart disease

Left-sided atrial or ventricular disease

Left-sided valvular disease

III. Pulmonary hypertension associated with lung disease

Chronic obstructive pulmonary disease

Interstitial lung disease

Other

IV. Pulmonary hypertension due to chronic thromboembolic disease

V. Miscellaneous

Diagnosis

S/Sx: vague, dyspnea with exertion (most common)

Class II: orthopnea, nocturnal dyspnea

Angina and syncope when right ventricular output is fixed

Chest radiography shows enlarged pulmonary hilar arteries and attenuated peripheral markings; disclose parenchymal causes of hypertension

Diagnosis is by echocardiography and is confirmed by right-sided catheterization, which usually may be deferred during pregnancy

Pulmonary Hypertension and Pregnancy

Idiopathic- worst prognosis

Pregnancy is contraindicated with severe disease, especially those with pulmonary arterial changes—most class I. With milder degrees of other causes—class II being common—the prognosis is much better

MARFAN’S SYNDROME :

Autosomal dominant genetic disorder with high dregree of penetrance

caused by abnormal fibrillin—a constituent of elastin—caused by any of dozens of mutations in the FBN1 gene located on chromosome 15q21

Weakened connective tissue

Cardiac manifestation : weakness of aortic root and mitral valve prolapse

(+) dilated aortic root prior to pregnancy : maternal mortality ~50% during pregnancy

Aortic root diameter >40mm : risk of aortic dissection

If 50-60 mm elective surgery before pregnancy

Aortic dilatation and dissecting aneurysm are the most serious abnormalities

Management :

prevent HPN

Beta blockers

Regional anesthesia : well tolerated

MITRAL VALVE PROLAPSE :

Dx: presence of a pathological connective tissue disorder—often termed myxomatous degeneration—which may involve the valve leaflets themselves, the annulus, or the chordae tendineae

Most common cardiac lesion in women

Incidence : ~ 12%

Most patients are asymptomatic and have uneventful pregnancies

B-blockers - given to decrease sympathetic tone, relieve chest pain and palpitations, and reduce the risk of life-threatening arrhythmias

Endocarditis prophylaxis is not indicated unless there is a coexistent mitral insufficiency

Other Cardiac Conditions

Coronary Artery Disease

Peripartal Cardiomyopathy

cardiomegaly

presence of S3

jugular distention

mitral or tricuspid regurgitation

diastolic or late systolic murmurs

cool extremities

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Peripartum Cardiomyopathy

diagnosis of exclusion following a contemporaneous cardiac evaluation of peripartum heart failure

similar to idiopathic dilated cardiomyopathy encountered in nonpregnant adults

Diagnostic Criteria

1. Development of heart failure in the last month of pregnancy or within 5 months after delivery.

2. Absence of an identifiable cause for the heart failure. 3. Absence of recognizable heart disease prior to the last month of

pregnancy. 4. Left ventricular dysfunction demonstrated by 2D Echo

such as depressed ejection fraction

Idiopathic Cardiomyopathy in Pregnancy

After exclusion of an underlying cause for heart failure, the default diagnosis is idiopathic or peripartum cardiomyopathy

Women with cardiomyopathy present with signs and symptoms of congestive heart failure.

Dyspnea is universal, and other symptoms include orthopnea, cough, palpitations, and chest pain

hallmark finding usually is impressive cardiomegaly

Hypertrophic Cardiomyopathy

Concentric left ventricular hypertrophy may be familial, and there also is a sporadic form not related to hypertension, termed idiopathic hypertrophic subaortic stenosis

Characterized by: cardiac hypertrophy, myocyte disarray, and interstitial fibrosis—is caused by mutations in any one of more than a dozen genes that encode proteins of the cardiac sarcomere

autosomal dominant

abnormality is in the myocardial muscle, and it is characterized by left ventricular myocardial hypertrophy with a pressure gradient to left ventricular outflow

Dx: established by echocardiographic identification of a hypertrophied and nondilated left ventricle in the absence of other cardiovascular conditions

Management:

Strenuous exercise prohibited during pregnancy

Abrupt positional changes are avoided to prevent reflex vasodilation and decreased preload

B adrenergic/Ca channel – given if symptoms develop like angina

Spinal analgesia - contraindicated

General Principles of Antenatal Management

1. All pregnant patients with heart disease should be asked to limit their physical activities based on classification.

2. Sexual activity is not contraindicated in patients in Class II. 3. A high protein, low salt (2 gms/day) has been recommended by

some authorities but the low sodium recommendation have not been shown to be useful except, in severe cases of congestive heart failure in the hospital setting and in those on diuretics for their predisposition to hypokalemia.

4. Routine supplementation with folic acid and iron sulfate is recommended as tolerated.

5. Anticoagulant drugs may be needed in pregnancy because of recurrent deep vein thrombosis, pulmonary embolism, rheumatic heart disease with atrial fibrillation, prosthetic valves or cyanotic congenital heart disease.

Timing of Delivery

Current NYHA functional status (hemodynamic compensation)

Fetal compromise (fetal growth restriction

Oligohydramnios or nonreassuring fetal tracing

Functional status trend over time

Possibility of improving or relieving the current functional status through optimization of treatment

evaluation of compliance

adjustment of medication doses or additional medications

additional rest

(Gei, 2001)

Management Principles during Delivery

Relief of pain

Outlet forceps delivery to avoid the Valsalva maneuver

Available blood for transfusion

Prophylactic antibiotics (for valvular problems)

Maintain patients in Fowler’s and semi-recumbent position

Maintain on continuous oxygen inhalation

Infective Endocarditis

infection involves cardiac endothelium and produces vegetations that usually deposit on a valve

Subacute bacterial endocarditis due to a low-virulence bacterial infection superimposed on an underlying structural lesion

most common causative organisms are streptococci—especially viridans—followed by Staphylococcus aureus and Enterococcus

IV drug abusers S. aureus is the predominant organism. Staphylococcus epidermidis commonly causes prosthetic valve infections

Streptococcus pneumoniae and Neisseria gonorrhoeae cause acute, fulminating disease

Antepartum endocarditis has been described with Neisseria sicca and Neisseria mucosa, the latter causing maternal death

Dx: fever, murmur, Anorexia, fatigue, and other constitutional symptoms are common, and the illness is frequently described as "flulike

embolic lesions, including petechiae, focal neurological manifestations, chest or abdominal pain, and ischemia in an extremity

Mgt:

Most viridans streptococci are sensitive to penicillin G given intravenously with gentamicin for 2 weeks

women allergic to penicillin are either desensitized or given intravenous ceftriaxone or vancomycin for 4 weeks

Staphylococci, enterococci, and other organisms are treated according to microbial sensitivity for 4 to 6 weeks

Prosthetic valve infections are treated for 6 to 8 weeks

Right-sided infections caused by methicillin-resistant S. aureus (MRSA) vancomycin

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Endocarditis Prophylaxis

2 gms Ampicillin and 1.5mg/kg Gentamicin, 30 mins. prior to the procedure, followed by 1 gm of Ampicillin as a second dose

High Risk Patients

1. Prosthetic cardiac valves (bioprosthetic and homograft)

2. Previous bacterial endocarditis 3. Complex cyanotic congenital heart disease

(Fallot or TGA) 4. Surgically corrected systemic pulmonary

shunts or conduits

Moderate Risk Category

1. Other congenital heart disease 2. Acquired valvular dysfunction 3. MVP with regurgitation or thickened

leaflets

Negligible Risk

Management Principles during Post-Partum Period

Maintain on hospital confinement for at least another week

Avoid extra exertion, maintain on bed rest

Massage uterus to avoid atony

Note : Italicized words were lifted from the book. Cardiac arrthymias and ischemic heart diseases were not included in the trans.

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References:

Cunningham et al. William’s Obstetrics: 23rd ed, chap44. McGraw Hill Publishing. 2010.

Dra Pascual’s lec

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“That in all Things, God may be Glorified”

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