Left subclavian artery stenosis with subclavian-subclavian bypass.
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Aortography↗
Biomedical subjects
I A Alhaddad
Publications and source records attributed to I A Alhaddad.
A remarkable medical story: benefits of angiotensin-converting enzyme inhibitors in cardiac patients.
The development of angiotensin-converting enzyme inhibitors (ACE inhibitors) has been one of the most remarkable stories in the treatment of cardiovascular diseases. Angiotensin converting enzyme inhibitors have several acute and sustained hemodynamic effects that are beneficial in the presence of left ventricular (LV) dysfunction. They increase cardiac output and stroke volume and reduce systemic vascular resistance as well as pulmonary capillary wedge pressure. The hemodynamic benefits are associated with improvement in the signs and symptoms of congestive heart failure (CHF) as well as decreased mortality, regardless of the severity of CHF. In patients with asymptomatic LV dysfunction, therapy with ACE inhibitors prevented the development of CHF and reduced hospitalization and cardiovascular death. They also increase survival when administered early after an acute myocardial infarction (MI). Most recently, ACE inhibition was associated with improved clinical outcomes in a broad spectrum of high-risk patients with preserved LV function. The mechanism of ACE inhibitors benefits is multifactorial and includes prevention of progressive LV remodeling, prevention of sudden death and arrhythmogenicity and structural stability of the atherosclerotic process. Evidence suggests that ACE inhibitors are underutilized in patients with cardiovascular diseases. Efforts should be directed to prescribe ACE inhibitors to appropriate patients in target doses. It is reasonable to believe that ACE inhibitors have a class effect in the management of LV dysfunction with or without CHF and acute MI. Whether the same is true for ACE inhibitors in the prevention of ischemic events is not known yet.
Angiotensin-Converting Enzyme Inhibitors↗
Late coronary artery reperfusion has additive beneficial effects on infarct expansion when combined with early angiotensin converting enzyme inhibitor therapy post myocardial infarction.
BACKGROUND: Individually, late coronary artery reperfusion and early angiotensin converting enzyme (ACE) inhibitor therapy prevent infarct expansion post myocardial infarction (MI). OBJECTIVES: To examine the effect of late reperfusion on infarct expansion when added to early ACE inhibitor therapy post MI. METHODS: Rats were randomized into two groups: Reperfusion group: rats underwent coronary artery occlusion followed by reperfusion 2 hours after MI, a time too late to reduce infarct size. A control group: rats underwent permanent coronary artery occlusion followed by a sham operation 2 hours after MI. All rats received enalapril (2.0 +/- 0.2 mg/kg) daily in drinking water, started immediately after the second operation. Rats were sacrificed 2 weeks after coronary occlusion. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarct size was similar in the reperfusion and control groups (23 +/- 2 vs 26 +/- 2%, p = NS). Septal thickness was also similar in both groups (1.8 +/- 0.1 vs 1.8 +/- 0.1 mm, p = NS). There was a trend towards thicker infarcts in the reperfusion group compared to the control group (0.84 +/- 0.06 vs 0.72 +/- 0.05 mm, p = 0.1). Compared to early ACE inhibition alone, late reperfusion combined with early ACE inhibition limited infarct expansion (expansion index, 1.13 +/- 0.12 vs 1.44 +/- 0.14, p < 0.05), prevented left ventricular (LV) dilation (LV volume, 0.30 +/- 0.02 vs 0.39 +/- 0.03 ml, p < 0.01) and prevented LV hypertrophy (LV weight, 0.71 +/- 0.18 vs 0.77 +/- 0.20 gm, p < 0.05). CONCLUSIONS: Late coronary artery reperfusion prevents infarct expansion, LV dilation and hypertrophy even when added to early ACE inhibitor therapy post MI. This suggests that late reperfusion may be beneficial in patients with acute MI treated with early ACE inhibitor therapy.
Angiotensin-Converting Enzyme Inhibitors↗
Renal artery stenosis in minority patients undergoing diagnostic cardiac catheterization: prevalence and risk factors.
BACKGROUND: Atherosclerotic renal artery stenosis (RAS) is a frequently overlooked clinical entity that can cause progressive renal failure and uncontrolled hypertension. Revascularization of a stenosed renal artery is associated with improved clinical outcomes including the prevention of renal failure. Thus, it is important to recognize all potential candidates for renal artery revascularization. In a general population referred for diagnostic cardiac catheterization, RAS of any severity was found in 30% of patients and significant stenosis (> or = 50% diameter narrowing) was found in 15% of patients. The number of minority groups is increasing in the US population, and RAS in this population is not well investigated. Our purpose was to determine the prevalence and risk factors associated with RAS in minority patients referred for diagnostic cardiac catheterization. METHODS: Abdominal aortography was performed in 171 consecutive minority patients referred for diagnostic cardiac catheterization (hispanics = 115, African Americans = 56). The association of clinical and angiographic variables with RAS was examined using univariate and multivariate logistic regression analyses. RESULTS: Renal artery stenosis of any severity was identified in 13.5% of patients (unilateral 7.7%, bilateral 5.8%). Significant RAS was found in 7.7% of patients (unilateral 4.8%, bilateral 2.9%). Independent predictors of RAS included age (mean +/-1SD, 68 +/-10 vs 57 +/-12 yr, P < 0.001, for patients with vs without RAS), coronary artery disease, and elevated serum creatinine levels (> 115 micromol/L). Race/ethnicity (hispanics vs African Americans), sex, smoking, congestive heart failure, diabetes mellitus, peripheral vascular disease, and hypertension were not independent predictors. CONCLUSIONS: Renal artery stenosis in minority patients undergoing diagnostic cardiac catheterization is less common than reported in white patients, is similar in hispanics and African Americans, and is similar in women and men. The clinical and angiographic features are helpful in predicting its presence.
Black or African American↗
Ventricular free wall rupture in acute myocardial infarction.
Despite a progressive reduction in acute myocardial infarction mortality over the years, death related to ventricular free wall rupture has not changed. This is mostly related to the catastrophic presentation and death within minutes in the majority of these patients. Once rupture is suspected, bedside echocardiography should be performed immediately, followed by pericardiocentesis and repair of the rupture site as quickly as possible. Measures to prevent cardiac rupture include the administration of beta-blockers and angiotensin-converting enzyme inhibitors unless contraindications exist, and the avoidance of steroidal and nonsteroidal anti-inflammatory agents such as ibuprofen and indomethacin.
Aged↗
Early angiotensin converting enzyme inhibitor therapy enhances the benefits of late coronary artery reperfusion on infarct expansion.
BACKGROUND: Individually, both late reperfusion and early angiotensin converting enzyme (ACE) inhibitor treatment prevent infarct expansion after acute myocardial infarction. OBJECTIVE: To examine the effect and mechanism of early post-myocardial infarction ACE inhibitor treatment, when used in combination with late coronary artery reperfusion, on infarct expansion. METHODS: Sprague-Dawley rats underwent 8 h of coronary occlusion followed by permanent reperfusion. The treatment group received enalapril, started 1 h after coronary occlusion and continued for 13 days. A control group received placebo. Two weeks after acute myocardial infarction, hemodynamic, morphometric and histologic analyses were performed. RESULTS: Hemodynamic parameters were similar in both groups (P = NS). Infarct size was similar in the ACE inhibitor and placebo treatment groups (44 +/- 4% compared with 39 +/- 4%, P = NS). Septal thickness was also similar in the two groups (2.8 +/- 0.3 mm compared with 2.7 +/- 0.3 mm, P = NS). The ACE inhibitor-treated group had thicker infarcts than those in the placebo-treated group (0.93 +/- 0.07 mm compared with 0.76 +/- 0.04 mm, P < 0.05) and these infarcts were less expanded (expansion index 1.17 +/- 0.12 compared with 1.57 +/- 0.12, P < 0.05). ACE inhibitor treatment was associated with hypertrophy of viable myocytes within the scar compared with placebo treatment (cell diameter 11.1 +/- 0.5 microns compared with 8.9 +/- 0.4 microns, P < 0.01). CONCLUSIONS: Early post-myocardial infarction ACE inhibitor treatment enhances the benefits of late coronary reperfusion on infarct expansion. The benefits may be related to hypertrophy of still-viable myocytes within the infarcted zone.
Angiotensin-Converting Enzyme Inhibitors↗
Late coronary artery reperfusion: benefits and mechanisms.
In patients with acute myocardial infarction (AMI), coronary artery reperfusion beyond 4 to 6 h after the onset of symptoms is believed to have little or no effect on infarct size. However, benefits have been demonstrated even when reperfusion is performed late and without significant myocardial salvage. Late reperfusion prevents infarct expansion and left ventricular remodelling. The mechanism is multifactorial and partially related to salvage of small islets of still viable myocytes within the scar. Other benefits of late reperfusion are electrical stability and prevention of arrhythmias. The survival benefits of reperfusion are strongly dependent on the time after the onset of symptoms until treatment (better outcomes are obtained with earlier reperfusion). Based on the demonstration of a significant reduction in mortality, the current practice is to perform reperfusion up to 12 h after the onset of symptoms. The survival benefits of reperfusion performed 13 to 24 h after the onset of AMI are less certain; however, large AMIs, particularly anterior infarcts, have the maximum risk of remodelling. Thus, benefits of reperfusion on left ventricular remodelling, arrhythmogenicity and prevention of congestive heart failure justify reperfusion in this group of patients up to 24 h after the onset of symptoms.
Animals↗
Chronic heart failure and the quality of life.
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Cardiotonic Agents↗
Pregnancy-induced severe left ventricular systolic dysfunction in a patient with hypertrophic cardiomyopathy.
This paper reports the first case of hypertrophic cardiomyopathy (HCM) that developed postpartum congestive heart failure (CHF) and severe left ventricular (LV) systolic dysfunction. Review of the literature and clinical implications are discussed.
Adult↗
Early exercise after experimental myocardial infarction: effect on left ventricular remodeling.
BACKGROUND: The effect of exercise on left ventricular remodeling after myocardial infarction is unclear. The purpose of this investigation was to test whether exercise undertaken during the healing phase of an acute myocardial infarction has an adverse effect on left ventricular remodeling. METHODS: Before surgery, rats (n = 94) were allocated randomly to one of four groups: 1) infarct, swimming exercise; 2) infarct, no exercise; 3) sham operation, swimming exercise; 4) sham operation, no exercise. Beginning 1 week after infarction or sham operation, the rats in the exercise groups swam twice daily for 2 weeks. After a deconditioning period of 5 days, the rats were re-anesthetized, hemodynamic measurements were made, and the hearts were fixed for morphometric analysis. RESULTS: Swimming exercise had no effect on remodeling of infarcted myocardium. Rats with infarcts in the swimming and no exercise groups had similar infarct thicknesses (1.1 +/- 0.2 mm and 0.8 +/- 0.2 mm respectively; NS), and similar degrees of infarct expansion (expansion index 1.2 +/- 0.3 and 1.4 +/- 0.3 respectively; NS). Swimming exercise also had no effect on remodeling of non-infarcted myocardium. Left ventricular volumes and pressure-volume relationships were similar in exercised and non-exercised infarcted rats. CONCLUSION: In rats, 2 weeks of swimming exercise, started 1 week after acute experimental myocardial infarction and followed by 5 days of deconditioning, does not have an adverse effect on left ventricular remodeling.
Analysis of Variance↗
Early angiotensin converting enzyme inhibitor therapy after experimental myocardial infarction prevents left ventricular dilation by reducing infarct expansion: a possible mechanism of clinical benefits.
OBJECTIVE: To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND: ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS: Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS: Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.
Angiotensin-Converting Enzyme Inhibitors↗
Benefits of late coronary artery reperfusion on infarct expansion progressively diminish over time: relation to viable islets of myocytes within the scar.
To define the time limit and mechanism of the effects of late coronary artery reperfusion on infarct expansion, rats were randomized into one of four groups: permanent left coronary artery occlusion; and 2, 8, and 16 hours of left coronary artery occlusion followed by reperfusion. Two weeks after coronary occlusion, morphometric and histologic analyses were performed. Benefits of late reperfusion on infarct expansion progressively diminished after increasingly long periods of coronary occlusion and were minimal but present after 16 hours of coronary occlusion. The extent of the benefits of late reperfusion on infarct expansion were related to preservation and hypertrophy of small islets of still viable myocytes located mainly in the subepicardium of the scar.
Analysis of Variance↗
Aspirin enhances the benefits of late reperfusion on infarct shape. A possible mechanism of the beneficial effects of aspirin on survival after acute myocardial infarction.
BACKGROUND: The time window of the benefits of late reperfusion on infarct shape is limited. In rats, these benefits diminish in a wave front over time, with minimal benefits when reperfusion follows 16 hours of coronary occlusion. The mechanism of the benefits of aspirin on survival after acute myocardial infarction is unknown. The purpose of this study was to test the ability of aspirin to enhance the benefits of late coronary artery reperfusion on infarct shape and to examine the mechanism of the benefits of aspirin on infarct shape. METHODS AND RESULTS: Rats were entered into two different protocols, the morphometric and the histological protocols. In the morphometric protocol, rats were randomized into two groups: the aspirin group, in which rats underwent left coronary artery occlusion followed by treatment with aspirin (12 mg/kg i.v.), and the control group, in which rats underwent left coronary artery occlusion followed by treatment with placebo. Rats in both groups were reperfused 8 hours after coronary occlusion. Rats in the aspirin group received aspirin in the drinking water (12 +/- 2 mg/kg daily). Morphometric analysis was performed 2 weeks after acute myocardial infarction. In the histological protocol, rats underwent the same randomization, coronary occlusion, and reperfusion protocols. Hearts were removed 24 hours after coronary occlusion, and microvessels were assessed for patency. Infarct size expressed as a percent of circumference was similar in the aspirin and placebo treatment groups (28 +/- 2% versus 33 +/- 3%, P = NS). Septal thickness was also similar in both groups (1.8 +/- 0.1 versus 2.1 +/- 0.1 mm, P = NS for aspirin versus placebo). The aspirin-treated group had thicker infarcts compared with the placebo-treated group (0.8 +/- 0.1 versus 0.5 +/- 0.1 mm, P < .05) and less expanded infarcts (expansion index, 1.2 +/- 0.1 versus 2.0 +/- 0.2, P < .05). Aspirin was associated with increased patency of the microvessels in the infarcted area compared with the placebo group (96% versus 64% of microvessels patent, P < .001). CONCLUSIONS: Aspirin enhances the benefit of late coronary artery reperfusion on infarct shape after 8 hours of coronary occlusion. The benefits of aspirin on infarct shape after late reperfusion are related to increased patency of the microvessels in the infarcted area.
Animals↗
Treatment of mitral stenosis.
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Catheterization↗
Does magnesium modify left ventricular remodeling after experimental myocardial infarction?
BACKGROUND: Magnesium therapy has been shown to improve survival and decrease the incidence of left ventricular failure when given to patients shortly after a myocardial infarction, but the mechanisms are unknown. We tested the hypothesis that the benefits of magnesium therapy are due to a favorable effect on early left ventricular remodeling, particularly on infarct shape changes. METHODS: Rats were infarcted and randomly allocated to two groups: group 1 (n = 8) received intravenous magnesium sulfate (200 mumol/kg) over 10 min started 30 min after coronary ligation, then an intraperitoneal dose (800 mumol/kg), which was repeated 6 h later. Group 2 (n = 10) served as a control group, and received normal saline. Using this regimen, the trough level of ionized magnesium 12 h after the intravenous dose was 33% above the control level. Three weeks after infarction, the hearts of the rats were arrested with saturated potassium chloride and fixed in formalin at 7.5 mmHg. The hearts were cut transversely into four slices. Photographs of both sides of each slice were taken and projected for morphometric analysis. RESULTS: Infarct size was similar in the magnesium and control groups (35 +/- 4 versus 30 +/- 2%). Infarct thickness, expansion index, and cavity area were also similar in both groups. CONCLUSIONS: Magnesium has no effect on early left ventricular remodeling or infarct expansion. The mechanism of its clinical benefits remains unexplained.
Animals↗
Cardiogenic shock due to huge right atrial thrombus.
An unusual case is reported of right atrial thrombus associated with cardiogenic shock. The role of two-dimensional echocardiography in detection of blood clots is highlighted.
Echocardiography↗