1/89. Thrombolysis with resolution of pulmonary hypertension in a heart transplant candidate.We report a patient with idiopathic cardiomyopathy and high pulmonary resistance due to pulmonary emboli of unknown age. Successful thrombolytic therapy returned his pulmonary resistance to normal, allowing orthotopic cardiac transplantation. This case underscores the need to aggressively diagnose and treat pulmonary emboli in potential transplant candidates.- - - - - - - - - - ranking = 1keywords = hypertension (Clic here for more details about this article) |
2/89. Severe hypertensive sequelae in a child with Seckel syndrome (bird-like dwarfism).We report a 19-year-old male with Seckel syndrome (bird-like dwarfism) who presents with malignant hypertension associated with hypertensive nephrosclerosis, dilated cardiomyopathy, and a ruptured cerebral artery aneurysm. Although end-organ injury due to chronic hypertension occurs frequently in adults, no previous reports of renal insufficiency due to hypertension exist in children or adolescents. We speculate that this patient may have been particularly prone to hypertensive end-organ injury due to his extreme short stature.- - - - - - - - - - ranking = 0.75keywords = hypertension (Clic here for more details about this article) |
3/89. A depressed myocardium.BACKGROUND: Venlafaxine is a potent neuronal serotonin and noradrenaline re-uptake inhibitor, and to a lesser extent an inhibitor of dopamine reuptake. paroxetine is a potent selective inhibitor of serotonin reuptake. CASE REPORT: A 27-year-old man ingested 1987.5 mg of venlafaxine and 360 mg of paroxetine. He subsequently developed systolic and diastolic hypertension, transient electrocardiographic abnormalities, and an area of persistent myocardial damage. He recovered from his overdose with his blood pressure and electrocardiogram returning to normal. The area of myocardial damage was documented on echocardiogram as an area of marked hypokinesia at the basal anterior septum. Despite the absence of confirming blood levels or the absolute exclusion of cocaine, this case indicates that venlafaxine and paroxetine have the potential for serious cardiotoxicity when taken in overdose.- - - - - - - - - - ranking = 0.42813151264909keywords = hypertension, blood pressure, pressure (Clic here for more details about this article) |
4/89. exercise training with a heart device: a hemodynamic, metabolic, and hormonal study.PURPOSE: The mechanisms of the training-induced improvements in left ventricular assist (LVAD) patients are unknown. methods: We measured the hemodynamic, gas exchange, and metabolic and hormonal effects of 6-wk exercise training in a cardiogenic shock patient who was assisted by an LVAD. RESULTS: After training, the peak power and VO2 increased by 166% and 56%, respectively (80 W and 16.1 mL x min(-1) x kg(-1)), whereas the ventilatory drive decreased. Although the LVAD output increased little with exercise, the systemic cardiac output rose (adequately for the VO2) from 5.91 and 4.90 L x min(-1) at rest to 9.75 and 9.47 L x min(-1) at peak work rate, before and after training, respectively. Thus, the left ventricle ejected again through the aortic valve. Unloading and/or retraining resulted in a left ventricular filling pressure decrease. Although the right ventricular ejection fraction increased with exercise, it decreased again at the maximal load after training. For a given work rate the arterial lactate, the norepinephrine (NE) and epinephrine (E) concentrations fell after training, but the enhanced maximal work rate elicited higher NE and E concentrations (4396 and 1848 pg x mL(-1), respectively). The lack of right ventricular unloading might have kept the atrial natriuretic peptide higher after training, but the blood cyclic gmp and endothelin were lower after training. CONCLUSION: In an LVAD patient, retraining returns the exercise capacity to the class III level by peripheral and left ventricular hemodynamic improvements, but the safety of maximal exercise remains to be proven in terms of right ventricular function and orthosympathetic drive.- - - - - - - - - - ranking = 0.065500854788843keywords = pressure (Clic here for more details about this article) |
5/89. Outpatient management of heart failure.The outpatient treatment of heart failure can be divided into 2 broad categories: older therapies, which improve hemodynamics, and newer therapies, which increase survival and improve function. Hemodynamic "triple" therapy includes digoxin to increase cardiac inotropy, antihypertensives to lower systolic pressure, and diuretics to remove fluid and decrease filling pressures. disease-modifying therapy requires the use of specific agents to lower blood pressure (angiotensin-converting enzyme inhibitors, angiotensin ii blockers, spironolactone, or hydralazine and nitrates) and beta-adrenergic blockade with carvedilol. The success of these newer therapies suggests that the standard triple therapy for heart failure should be expanded to "quadruple" therapy that includes carvedilol.- - - - - - - - - - ranking = 0.30913322222678keywords = blood pressure, pressure (Clic here for more details about this article) |
6/89. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. angina pectoris-myocardial infarction Investigations in japan.OBJECTIVES: To determine the clinical features of a novel heart syndrome with transient left ventricular (LV) apical ballooning, but without coronary artery stenosis, that mimics acute myocardial infarction, we performed a multicenter retrospective enrollment study. BACKGROUND: Only several case presentations have been reported with regard to this syndrome. methods: We analyzed 88 patients (12 men and 76 women), aged 67 /- 13 years, who fulfilled the following criteria: 1) transient LV apical ballooning, 2) no significant angiographic stenosis, and 3) no known cardiomyopathies. RESULTS: Thirt-eight (43%) patients had preceding aggravation of underlying disorders (cerebrovascular accident [n = 3], epilepsy [n = 3], exacerbated bronchial asthma [n = 3], acute abdomen [n = 7]) and noncardiac surgery or medical procedure (n = 11) at the onset. Twenty-four (27%) patients had emotional and physical problems (sudden accident [n = 2], death/funeral of a family member [n = 7], inexperience with exercise [n = 6], quarreling or excessive alcohol consumption [n = 5] and vigorous excitation [n = 4]). Chest symptoms (67%), electrocardiographic changes (ST elevation [90%], Q-wave formation [27%] and T-wave inversion [97%]) and elevated creatine kinase (56%) were found. After treatment of pulmonary edema (22%), cardiogenic shock (15%) and ventricular tachycardia/fibrillation (9%), 85 patients had class I New York Heart association function on discharge. The LV ejection fraction improved from 41 /- 11% to 64 /- 10%. Transient intraventricular pressure gradient and provocative vasospasm were documented in 13/72 (18%) and 10/48 (21%) of the patients, respectively. During follow-up for 13 /- 14 months, two patients showed recurrence, and one died suddenly. CONCLUSIONS: A novel cardiomyopathy with transient apical ballooning was reported. Emotional or physical stress might play a key role in this cardiomyopathy, but the precise etiologic basis still remains unclear.- - - - - - - - - - ranking = 0.065500854788843keywords = pressure (Clic here for more details about this article) |
7/89. Two cases of postpartum cardiomyopathy initially misdiagnosed for pulmonary embolism.PURPOSE: To underline the crucial role of urgent echocardiography in the differential diagnosis of acute respiratory and/or circulatory failure in the postpartum period. CLINICAL FEATURES: A 24-yr-old woman was admitted to the intensive care unit (ICU) with a preliminary diagnosis of pulmonary embolism (PE) one week after cesarean section. Neither computerized tomography nor Doppler sonography showed any signs of deep venous thrombosis or PE. In the ICU she required intubation and ventilatory support for acute respiratory and circulatory failure. Bedside echocardiography revealed features of left ventricular failure. A diagnosis of postpartum cardiomyopathy (PPCM) was made, appropriate treatment instituted and the patient soon improved. A 29-yr-old, previously healthy primipara presented at the Maternity Clinic on the fourth postpartum day complaining of increasing dyspnea and fatigue. Within eight hours she required intubation, ventilatory support and subsequent defibrillation due to cardiac arrest. She was transferred to the ICU with a preliminary diagnosis of PE. She developed pulmonary edema followed by cardiac arrest with successful resuscitation. Bedside echocardiography revealed a left ventricular ejection fraction below 30% with an increased systolic diameter of the left ventricle, restrictive diastolic abnormalities and no signs of pulmonary hypertension. Peripartum cardiomyopathy was diagnosed and supportive treatment for heart failure was instituted. CONCLUSION: It is possible to misdiagnose postpartum cardiomyopathy for PE. An error in diagnosis is life-threatening for the patient. echocardiography is a valuable tool in the differential diagnosis. As a noninvasive procedure, it should be performed at the bedside as soon as possible to institute proper treatment and to avoid potentially fatal errors.- - - - - - - - - - ranking = 0.25keywords = hypertension (Clic here for more details about this article) |
8/89. A rare cause of cardiogenic shock: catecholamine cardiomyopathy of pheochromocytoma.pheochromocytoma is a rare catecholamine secreting tumor that accounts for about 0.04% of cases of hypertension. Other less common cardiovascular manifestations such as arrhythmias, angina pectoris, acute myocardial infarction, dilated cardiomyopathy, acute heart failure, and cardiogenic shock have occasionally been reported. We describe the case of a 32-year-old previously healthy male patient who died of cardiogenic shock within 10 hours of admission. Postmortem examination showed a catecholamine cardiomyopathy and a pheochromocytoma of the right adrenal gland. pheochromocytoma with predominant epinephrine or dopamine secretion may take a hypotensive course. Sudden excessive catecholamine release can, as in the described case, cause cardiogenic shock.- - - - - - - - - - ranking = 0.25keywords = hypertension (Clic here for more details about this article) |
9/89. Sipple's syndrome presenting acutely as severe heart failure.We describe the case of a 56-year-old man who developed acute hypertension leading to cardiac insufficiency, arrhythmia, severe heart failure and death. The autopsy revealed Sipple's syndrome (multiple endocrine neoplasia syndrome type IIa) and catecholamine-induced cardiomyopathy. This man had received a false diagnosis of primary hypertension 1 year before. The prime objective of this report is to call attention to the necessity of an in depth diagnosis of labile and paroxysmal hypertension. The clinical diagnostic features of phaeochromocytoma as well as the main therapeutic approaches suggested in the literature are commented on.- - - - - - - - - - ranking = 0.75keywords = hypertension (Clic here for more details about this article) |
10/89. Bilateral pleural effusion and pulmonary edema caused by a fistulous aneurysm of the ductus arteriosus.We report an unusual case of pulmonary edema and rapid collection of bilateral pleural effusion caused by a fistulous large aneurysm of the ductus arteriosus (DAA). The diagnosis was performed by contrast CT and aortography. The cause of pulmonary edema and effusion was thought to be both elevated capillary pressure due to overload of the pulmonary circulation and decreased water clearance due to compression of the lymphatic system by the large DAA itself. Therefore, fistulous DAA should be considered when a continuous heart murmur and swelling in the aortic window are recognized. Once DAA is diagnosed, surgery should be performed without delay.- - - - - - - - - - ranking = 0.065500854788843keywords = pressure (Clic here for more details about this article) |
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