Idiopathic postpartum cardiomyopathy: Report of a case with special reference to its ultrastructural changes in the myocardium as studied by endomyocardial biopsy
“…Polymerase chain reaction (PCR) and extraction of genomic material from contrast MRI-guided EMB may help in successful detection of viral genomes 55. At the same time, there are several reports without any prevalence of viral infection in PPCM patients,2,8,25,46,48,60 and it has been argued that viral cardiomyopathy should not be included in PPCM criteria 3. Specific further study is essential to establish the relationship of viral myocarditis and PPCM.…”
Section: Etiologymentioning
confidence: 99%
“…Histological evidence of hypertrophy, degeneration, fibrosis, interstitial edema, fatty and mononuclear cell infiltration is seen in the myocardium with a sparse to abundant collection of eosinophils 1-4,8-10,14,45. Electron microscopy has revealed varying degrees of enlargement, destruction or fragmentation of myofibrils, an increase in size and number of mitochondria, glycogen and some abnormal pertinacious material deposits 1-3,45,60. Histochemical pictures of myocardial cells denote occasional sarcoplasmic fat vacuoles containing triglycerides without any accumulation of lipofuscin or amyloid 3.…”
Peripartum cardiomyopathy (PPCM) is a rare but serious form of cardiac failure affecting women in the last months of pregnancy or early puerperium. Clinical presentation of PPCM is similar to that of systolic heart failure from any cause, and it can sometimes be complicated by a high incidence of thromboembolism. Prior to the availability of echocardiography, diagnosis was based only on clinical findings. Recently, inclusion of echocardiography has made diagnosis of PPCM easier and more accurate. Its etiopathogenesis is still poorly understood, but recent evidence supports inflammation, viral infection and autoimmunity as the leading causative hypotheses. Prompt recognition with institution of intensive treatment by a multidisciplinary team is a prerequisite for improved outcome. Conventional treatment consists of diuretics, β blockers, vasodilators, and sometimes digoxin and anticoagulants, usually in combination. In resistant cases, newer therapeutic modalities such as immunomodulation, immunoglobulin and immunosuppression may be considered. Cardiac transplantation may be necessary in patients not responding to conventional and newer therapeutic strategies. The role of the anesthesiologist is important in perioperative and intensive care management. Prognosis is highly related to reversal of ventricular dysfunction. Compared to historically higher mortality rates, recent reports describe better outcome, probably because of advances in medical care. Based on current information, future pregnancy is usually not recommended in patients who fail to recover heart function. This article aims to provide a comprehensive updated review of PPCM covering etiopathogeneses, clinical presentation and diagnosis, as well as pharmacological, perioperative and intensive care management and prognosis, while stressing areas that require further research.
“…Polymerase chain reaction (PCR) and extraction of genomic material from contrast MRI-guided EMB may help in successful detection of viral genomes 55. At the same time, there are several reports without any prevalence of viral infection in PPCM patients,2,8,25,46,48,60 and it has been argued that viral cardiomyopathy should not be included in PPCM criteria 3. Specific further study is essential to establish the relationship of viral myocarditis and PPCM.…”
Section: Etiologymentioning
confidence: 99%
“…Histological evidence of hypertrophy, degeneration, fibrosis, interstitial edema, fatty and mononuclear cell infiltration is seen in the myocardium with a sparse to abundant collection of eosinophils 1-4,8-10,14,45. Electron microscopy has revealed varying degrees of enlargement, destruction or fragmentation of myofibrils, an increase in size and number of mitochondria, glycogen and some abnormal pertinacious material deposits 1-3,45,60. Histochemical pictures of myocardial cells denote occasional sarcoplasmic fat vacuoles containing triglycerides without any accumulation of lipofuscin or amyloid 3.…”
Peripartum cardiomyopathy (PPCM) is a rare but serious form of cardiac failure affecting women in the last months of pregnancy or early puerperium. Clinical presentation of PPCM is similar to that of systolic heart failure from any cause, and it can sometimes be complicated by a high incidence of thromboembolism. Prior to the availability of echocardiography, diagnosis was based only on clinical findings. Recently, inclusion of echocardiography has made diagnosis of PPCM easier and more accurate. Its etiopathogenesis is still poorly understood, but recent evidence supports inflammation, viral infection and autoimmunity as the leading causative hypotheses. Prompt recognition with institution of intensive treatment by a multidisciplinary team is a prerequisite for improved outcome. Conventional treatment consists of diuretics, β blockers, vasodilators, and sometimes digoxin and anticoagulants, usually in combination. In resistant cases, newer therapeutic modalities such as immunomodulation, immunoglobulin and immunosuppression may be considered. Cardiac transplantation may be necessary in patients not responding to conventional and newer therapeutic strategies. The role of the anesthesiologist is important in perioperative and intensive care management. Prognosis is highly related to reversal of ventricular dysfunction. Compared to historically higher mortality rates, recent reports describe better outcome, probably because of advances in medical care. Based on current information, future pregnancy is usually not recommended in patients who fail to recover heart function. This article aims to provide a comprehensive updated review of PPCM covering etiopathogeneses, clinical presentation and diagnosis, as well as pharmacological, perioperative and intensive care management and prognosis, while stressing areas that require further research.
“…Ritchie, in 1849, described heart failure in late pregnancy and the puerperium associated with a primary heart muscle disease [1]. In 1870, Virchow and Porak found myocardial degeneration to be a cause of death in women dying in the puerperium [2]. The condition was virtually forgotten until the 1930s when descriptions of women with heart failure in the post-partum period and autopsy findings of enlarged hearts with focal areas of necrosis emerged in the United States [3,4].…”
“…Many terms are used to describe this disorder, including toxic postpartal heart failure, postpartum heart disease, postpartum myocardosis, Meadows' syndrome, idiopathic myocardial degeneration associated with pregnancy, Zaria syndrome, and postpartum cardiomyopathy [4,[7][8][9][10].…”
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