Left ventricular hypertrophy in response to pressure overload is therefore a natural compensatory mechanism to reduce systolic wall tension. Systolic wall tension, like contractility and heart rate, cannot be estimated numerically. However, the importance lies in understanding the contributing factors and their directional change on myocardial oxygen consumption. Continue reading
Modern women leading an active lifestyle prefer not to bother about tiny things. They simply don’t have a spare minute for it: successful career, strong family, rich sexual life… The only thing they must be concerned about is contraception.
Sometimes it happens that a woman plans to get pregnant at a certain period of life and she uses every convenient method of contraception. The more so because there are plenty of fertility control remedies women are offered today. How can one find the most suitable method? It depends on your possibilities and preferences. Continue reading
Given the high prevalence of nonspecific abdominal pain in our population, drug-related causes for abdominal complaints must be carefully sought. Angioedema involving the gastrointestinal system should be considered in patients taking ACE inhibitors who present with acute and/or chronic abdominal symptoms, irrespective of the duration of therapy. AIAI is an important diagnosis because the dysutility of a delayed and/or missed diagnosis is considerable, and treatment options are simplistic and straightforward. Prompt radiological investigation(s) during the symptomatic phase is a key component to making the diagnosis. AIAI is completely reversible following the discontinuation of the offending ACE inhibitor. HA must be ruled out as an important comorbidity. ARAs should not be used as substitutes for the ACE inhibitors.
Although approximately half of the patients with AIAI had prior presentations involving facial and/or oropharyngeal swelling, no patient had concomitant airway compromise. However, a cautionary approach must be taken, and respiratory status must be closely monitored in these patients. Patients should continue to receive nothing by mouth, and be given supportive care and adequate fluid resuscitation, and the ACE inhibitor should be discontinued. The possible development of hypovolemia and small bowel obstruction must be closely monitored in the acute setting. However, in all nine cases described, symptoms resolved within 24 to 48 h without the need for specific medical therapy. In particular, there is no role for antihistamine or corticosteroids during the acute symptomatic period. The reversible nature of the disorder is clearly revealed by the prompt resolution of symptoms once the diagnosis is made and the offending drug discontinued.
Routine evaluations should include hematological, biochemical, microbiological and radiological investigations as well as ascitic fluid analysis. Inadequate inhibition of the first component of human complement (C1-INH) gives rise to HA and an acquired form of angioedema. HA is commonly diagnosed when patients present with recurrent gastrointestinal symptoms and bowel edema. As such, complement (C3, C4 and CH50), C1q and C1-INH levels should always be measured with samples taken during the symptomatic period to increase the diagnostic yield. Moreover, the diagnosis of HA, irrespective of the use of ACE inhibitor, has important and unique management strategies. When radiological studies reveal large bowel involvement, a colonoscopy with mucosal biopsy is beneficial in excluding diagnoses of an inflammatory and/or vascular origin.
AIAI was diagnosed based on the temporal relationship between the use of an ACE inhibitor, absence of alternative diagnoses and the resolution of symptoms upon discontinuation of the ACE inhibitor. A follow-up assess-ment(s) with a repeat radiological procedure (abdominal CT or ultrasound) is of critical importance in the postdischarge period to confirm a complete resolution of the ascites and bowel wall edema and to substantiate the diagnosis. A rechallenge with an ACE inhibitor should not be attempted.
A total of 13 case reports describing AIAI have revealed several characteristic features of the disease. Patients often have recurrent episodes of abdominal complaints and are sometimes given an alternative diagnosis with occasional surgical intervention. The time of diagnosis varied from a few hours to seven years following the initiation of ACE inhibitor, with over 75% of patients (10 of 13 patients) having a delayed diagnosis (two months or longer), and was independent of the dose of ACE inhibitor. This was likely due to a delay in presentation and/or diagnosis. Patients reported a chronic use of ACE inhibitors associated with recurrent gastrointestinal symptoms and multiple episodes of acute exacerbations. Gastrointestinal symptoms in patients taking ACE that cannot be explained by other more common causes should prompt physicians to consider AIAI, irrespective of the duration of therapy. In addition, several patients had prior episodes of angioedema involving the face and/or oropharynx. As such, a diagnosis of ACE inhibitor-induced angioedema of the face and/or oropharynx does not preclude the possibility of AIAI.
The precipitation of angioedema involves an interaction of environmental triggers in genetically susceptible individuals. The pathophysiological mechanisms involve an interaction between immunological factors, complement pathways and various peptidergic and aminergic byproducts. AIAI has been described with a range of ACE inhibitors, which suggests that the pathophysiology is closely related to their pharmacological mechanisms of action rather than to idiosyncratic drug reactions (Table 2). ACE and NEP inhibition are associated with a reduction in the metabolism of bradykinin and substance P, leading to accumulation of these peptides in the plasma and/or tissues. By using a sensitive assay, plasma bradykinin levels were shown to have a greater than 10-fold increase in patients with hereditary and ACE-inhibitor induced angioedema. The final common pathway culminates in angioedema and exudative ascites due to uncontrolled vasodilation, increased capillary permeability and extravasation of fluid from the visceral vasculature. Histological findings from biopsy of the intestine include normal findings and submucosal edema with intact villous architecture and the absence of cellular infiltrate. Angiotensin II receptor antagonists cause an increase in plasma angiotensin II levels, which may lead to a negative feedback inhibition of ACE activity, thus predisposing individuals to developing angioedema.
Despite the well-documented incidence of cutaneous and/or facial/oropharyngeal angioedema (see above), no study has systematically examined the incidence of AIAI in patients taking ACE inhibitors. Several lines of evidence suggest that angioedema of the intestine is underdiagnosed, and more recent data have highlighted the clinical importance of AIAI. First, acute nonspecific abdominal pain (NSAP) accounts for 13% to 40% of all emergency surgical admissions and is associated with an extensive series of investigations. Despite further investigations at substantial cost, about one-third of all patients with acute abdominal pain leave the hospital without a final diagnosis. Although drug-induced angioedema may be partly responsible for acute NSAP, most studies fail to report a detailed drug history.
A 37-year old woman with a prior history of gastrointestinal disorders presented to the emergency department with acute onset of painful abdominal cramps, nausea, and several episodes of vomiting and watery diarrhea. Her past medical history was remarkable for essential hypertension and chronic gastrointestinal complaints, with several visits to the emergency department. Two days before presentation, the dose of fosinopril (ACE inhibitor) was increased from 10 mg once daily to 30 mg once daily. She was also taking an oral contraceptive. She had no known allergies to drugs or environmental agents, and her travel history was negative. There was no family history for any diseases. The patient was afebrile, and no facial or oropharyngeal swelling was noted. Mild diffuse abdominal tenderness with bulging flanks and flank dullness were present.