Myocardial rupture occurs in the setting of acute myocardial infarction (AMI), blunt and penetrating cardiac trauma, primary cardiac infection, primary and secondary cardiac tumors, infiltrative diseases of the heart, and aortic dissection. The clinical presentation of myocardial rupture depends on the mechanism and site of injury and the hemodynamic effects of the rupture. Mortality rates are extremely high unless early diagnosis and surgical intervention are provided rapidly.
AMI is the most common etiology of myocardial rupture. Ischemic myocardial rupture may involve the left ventricular (LV) and right ventricular (RV) free walls, ventricular septum, and LV papillary muscle, in decreasing order of frequency. Myocardial rupture rarely involves the left or right atrial walls.
The consequences of myocardial rupture in the setting of AMI can include pericardial tamponade, ventricular septal defect (VSD) with left-to-right shunt, acute mitral regurgitation (MR), or formation of a pseudoaneurysm. In most instances, the catastrophic clinical presentation occurs within 3-5 days of a rather small AMI. Both hemodynamic factors (increased intracavitary pressure) and regional myocardial structural weakness (myocyte necrosis, collagen matrix resolution, intense inflammation) are important contributory factors to myocardial rupture in the setting of AMI.
In rare instances, patients have been reported to simultaneously experience LV free wall rupture and ventricular septal or papillary muscle rupture (double rupture) following AMI. In the case of a papillary muscle rupture, the posteromedial papillary muscle is twice as likely to rupture as is the anterolateral papillary muscle. This likelihood is because the anteromedial papillary muscle is more often supplied by 2 arterial systems (left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is frequently supplied by only one coronary artery (usually the right) system. Rupture of both papillary muscles following AMI has been reported.
In some patients who survive LV free wall rupture following AMI, the rupture can be sealed by the epicardium (visceral pericardium) or by a hematoma on the epicardial surface of the heart. This entity has been referred to as LV diverticulum or contained myocardial rupture and represents a subacute pathologic condition between free rupture into the pericardial cavity and formation of a pseudoaneurysm. A pseudoaneurysm is formed if the area of rupture is contained locally by the adjacent parietal pericardium and represents the chronic stage of LV free wall rupture. The most common etiology of LV pseudoaneurysm is AMI. (LV pseudoaneurysm is twice as common with inferior, rather than anterior, AMI.) LV pseudoaneurysms may develop following surgery, especially following mitral valve replacement.
Blunt cardiac trauma, most commonly in the setting of an automobile accident, may cause myocardial rupture as a result of cardiac compression between the sternum and the spine, direct impact (sternal trauma), or from deceleration injury. It may result in rupture of the papillary muscles, cardiac free wall, or the ventricular septum. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.
However, among those who reach the hospital alive, the right atrium is the most commonly involved chamber. In up to 30% of cases, the rupture involves more than one chamber. Delayed myocardial rupture has been reported as a result of cardiac contusion. Acute mitral or tricuspid regurgitation, VSD, or pericardial tamponade may result from myocardial rupture secondary to blunt cardiac trauma.
Penetrating myocardial injury occurs most commonly as a result of stab or gunshot wounds. Unlike blunt trauma, penetrating cardiac injury always involves the pericardium. Consequently, ventricular free-wall rupture in this setting may result in either pericardial tamponade (if the pericardial wound is obliterated) or intrathoracic hemorrhage. While pericardial tamponade is more common with stab wounds, gunshot wounds more frequently are associated with hypovolemic shock. The cardiac chambers involved are, in decreasing order of frequency, the right ventricle, left ventricle, right atrium, and left atrium.
Myocardial abscesses accompanying infective endocarditis may rupture transmurally, resulting in VSD or pericardial tamponade (pyohemopericardium). Such abscesses are observed most commonly in the setting of Staphylococcus aureus endocarditis involving prosthetic valves in the aortic position. Rarely, myocardial necrosis due to acute myocarditis, tuberculosis, or sarcoidosis may result in myocardial rupture.
Myocardial rupture is rarely caused by primary (hemangiopericytoma, angiosarcoma, lymphoma) or secondary (metastatic) cardiac tumors. Lymphomas and acute myeloblastic leukemia also have been associated with myocardial rupture.
Myocardial rupture complicates up to 10% of AMIs. Approximately 6-10% of penetrating chest wounds and 15-75% of blunt chest traumas are associated with cardiac injury. Myocardial rupture occurs in 10-15% of fatal motor vehicle accidents. Incidence of cardiac rupture following blunt trauma is 0.5-2% among hospital trauma admissions.
Myocardial rupture is responsible for nearly 15% of all in-hospital deaths among patients with AMI. It is the second most common cause, after pump failure, of in-hospital mortality among patients with AMI.
The overall mortality rate from myocardial rupture following blunt trauma is 76-93%. However, among those who reach the hospital alive, the mortality rate is 29-50%. Mortality from myocardial rupture resulting from penetrating trauma ranges from 62-89% in the field to 2-83% after reaching a hospital. The latter largely depends on the type of injury, rapidity of the transfer to a hospital, and patients' vital signs and condition upon arrival.
Following myocardial rupture as a result of penetrating cardiac trauma, hospital mortality is higher in those presenting with hypovolemia rather than pericardial tamponade (22% vs 8%). In-hospital mortality is lowest for patients with RV rupture.
Myocardial rupture after AMI is reported more commonly in women than in men (1.4:1).
Traumatic myocardial rupture is more common in males (up to 85% in some series) than in females.
Myocardial rupture after AMI is more common in patients aged 60 years or older.
Traumatic myocardial rupture is observed more commonly in those aged 15-63 years (mean, 34 y).
Myocardial rupture after AMI may occur from 1 day to 3 weeks after infarction. Most ruptures occur 3-5 days after infarction.
In most patients, myocardial rupture manifests as a catastrophic event (acute pulmonary edema, cardiogenic shock, or circulatory collapse) within days of a first, small, uncomplicated AMI.
Older women, especially those with recurrent postinfarction angina, and patients with systemic hypertension more commonly experience myocardial rupture following AMI.
Acute onset of shortness of breath, chest pain, shock, diaphoresis, unexplained emesis, cool and clammy skin, and syncope may herald the onset of ventricular septal rupture following AMI.
Sudden death due to LV free-wall rupture may be the first manifestation of coronary artery disease in a small percentage of patients with AMI.
Immediate, early, or delayed acute pulmonary edema (papillary muscle rupture), congestive heart failure (ventricular septal rupture), and hypotension (free-wall rupture) are the cardinal manifestations of myocardial rupture following blunt chest trauma. Concomitant rupture of the myocardium, pericardium, and diaphragm may result in the accumulation of blood in the abdominal cavity.
In patients with traumatic myocardial rupture, manifestations depend on the site, mode, and extent of cardiac injury.
Sudden death occurs shortly after the injury in most patients with traumatic myocardial rupture and is due to pericardial tamponade or exsanguination.
Cardiogenic or hypovolemic shock is the predominant manifestation of traumatic myocardial rupture in patients who reach a hospital.
Patients with pericardial tamponade may present with dyspnea, chest pain, hypotension, cold peripheries, and mental status changes.
A small percentage of patients with significant penetrating cardiac trauma have few or no symptoms upon presentation to a hospital.
Pseudoaneurysms may manifest as cerebral or systemic embolic events or sudden death (rupture). Hemoptysis may occur due to the formation of ventriculopulmonary fistulas. Approximately 10% of patients with pseudoaneurysm are asymptomatic.
Of those who sustain cardiac trauma from stab wounds, 18-35% remain without clinical signs of myocardial injury.
Papillary muscle rupture (partial or complete)
Acute pulmonary edema manifests as tachypnea, tachycardia, hypotension, respiratory distress, diffuse pulmonary rales, and signs of MR.
The MR murmur may be absent or atypical (soft and not holosystolic) due to rapid equalization of pressures between the left ventricle and left atrium. This equalization is due to the noncompliance of the acutely volume-overloaded left atrium (ie, the left atrial pressure increases sharply in response to sudden rise in volume).
Sudden unexplained hypotension and/or pulmonary edema in patients experiencing their first inferior AMI should raise the possibility of papillary muscle rupture, even in the absence of a murmur.
Left ventricle free-wall rupture
Post-AMI pericarditis manifested as pleuritic chest pain and friction rub may be present in some patients prior to onset of rupture and generally indicates transmural extension of the infarct. Cardiogenic shock due to pericardial tamponade manifests as sudden onset of bradycardia, clear lung fields, distended neck veins, Kussmaul sign (ie, paradoxical inspiratory increase in jugular venous pressure), muffled heart sounds, and pulsus paradoxus (ie, an inspiratory drop in systolic blood pressure of >10 mm Hg).
Hypovolemic shock may occur due to direct communication with the thoracic or abdominal cavity through a pericardial tear. This manifests as hypotension, tachycardia, cool and clammy extremities, pallor, and diaphoresis.
Ventricular septal rupture
Hypotension may be present.
Patients may have acute pulmonary edema.
A loud holosystolic murmur may be heard at the lower left sternal border or diffusely over the precordium and is often associated with a thrill.
Ventricular arrhythmias may be present.
A friction rub may be heard.
Pseudoaneurysms frequently rupture, resulting in cardiogenic or hypovolemic shock.
Some patients may have a systolic murmur due to the turbulent flow across the narrow neck of the pseudoaneurysm.
Systemic embolism that originates from the pseudoaneurysm may result in various cerebrovascular or systemic ischemic symptoms.
Arrhythmia may be present, especially ventricular tachycardia and fibrillation.
Acute myocardial infarction
Risk factors for myocardial rupture following AMI include a relatively small first AMI, female sex, age older than 60 years, hypertension, use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids during the acute phase of AMI (interference with the healing process), late thrombolysis (>11 h), postinfarct angina and elevated peak serum C-reactive protein.
Protective factors include LV hypertrophy, history of previous infarcts, congestive heart failure, history of chronic ischemic heart disease, early use of beta-blockers after AMI, and successful (and timely) primary percutaneous coronary intervention.
Trauma may be blunt or penetrating.
Trauma also may be iatrogenic in nature, resulting from (1) diagnostic catheterization, including transseptal puncture and endomyocardial biopsy; (2) balloon valvuloplasty; (3) pericardiocentesis; (4) placement of temporary or permanent pacing catheters; and (5) cardiac surgery, especially mitral valve replacement.
Rupture of a myocardial abscess or AMI secondary to coronary embolism of the vegetative material may occur in patients with infective endocarditis.
Other infections may include tuberculosis, echinococcal cysts, and myocarditis.
Primary cardiac tumors may be present.
Patients may have secondary or metastatic tumors of the heart.
Patients may have lymphoma or acute myeloblastic leukemia.
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Jumat, 08 Januari 2010
Diposting oleh FX di 19.51
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome