Dwight A. Dishmon

Fracture Risk in Men With Congestive Heart Failure: Risk Reduction With Spironolactone

OBJECTIVES The purpose of this study was to determine whether spironolactone use is associated with fractures in men with congestive heart failure (CHF). BACKGROUND In rats with aldosteronism, spironolactone preserves skeletal strength. However, in humans, the relationship of spironolactone to fractures is not known. METHODS The medical records of all male patients with CHF from 1999 to 2005 treated at the Veterans Affairs Medical Center, Memphis, Tennessee, were reviewed (n = 4,735). Odds ratios with 95% confidence intervals of having a fracture associated with spironolactone use were estimated using conditional logistic regression. RESULTS We identified 167 cases with a single-incident fracture and matched these by age and race to 668 control subjects without fractures. After adjustment for covariates, spironolactone use was inversely associated with total fracture (odds ratio: 0.575; 95% confidence interval: 0.346 to 0.955, p = 0.0324). CONCLUSIONS The use of spironolactone is inversely associated with fractures in men with CHF.

Secondary hyperparathyroidism in patients with untreated and treated congestive heart failure

Background:The congestive heart failure syndrome includes a systemic illness with wasting of soft tissues and bone. We hypothesized secondary hyperparathyroidism (HPT) would be found in hospitalized patients with decompensated congestive heart failure (CHF), where secondary aldosteronism is expected, and who were either untreated or treated medically. Methods:In 9 consecutive patients (7 males, 2 females; 8 African-American, 1 Caucasian; 33–60 yrs) admitted to the Regional Medical Center during a 28-day period with chronic left ventricular systolic dysfunction (EF<35%) and decompensated CHF (5 untreated; 4 treated with an angiotensin converting enzyme inhibitor, furosemide, and small-dose spironolactone), we measured: plasma parathyroid hormone (PTH); serum calcium corrected for albumin, magnesium, and phosphorus; serum creatinine and calculated creatinine clearance. Results:Plasma PTH was elevated above the normal range (6-65 pg/mL) in both untreated and treated patients with CHF (204±60 and 134±14 pg/mL, respectively). Serum corrected calcium was normal (8.4-10.2 mg/dL) in both untreated and treated CHF (9.7±0.l and 9.1±0.2 mg/dL, respectively) as were serum magnesium and phosphorus. Calculated creatinine clearance did not differ between untreated and treated patients (74±15 and 83±21 mL/min, respectively). Conclusions:Secondary HPT was found in 5 untreated and 4 treated patients consecutively hospitalized over a 28-day period with decompensated CHF. Corrected serum calcium was normal. Plasmaionized calcium, a determinant of PTH secretion, was not measured. Although vitamin D levels were not assessed, the presence of hypovitaminosis D in these housebound patients with symptomatic CHF cannot be discounted. HPT may contribute to the systemic illness that accompanies CHF, including bone wasting.

Successful aspiration and rheolytic thrombectomy of a renal artery infarct and review of the current literature.

The use of revascularization techniques including angioplasty, thrombectomy, and stenting in the coronary, cerebral, and peripheral arteries has revolutionized the entire field of endovascular therapeutics. In renal thromboembolism, the classic treatment has been anticoagulation with possible thrombolysis and surgical thrombectomy. The role of endovascular therapy in renal thromboembolism remains controversial. There are a few anecdotal reports about the use of aspiration and rheolytic thrombectomy in the renal arteries. We present a case of acute renal infarction resulting from systemic embolism secondary to atrial fibrillation. This was treated with revascularization, including aspiration and rheolytic thrombectomy, with excellent results.

Hypovitaminosis D and Valvular Calcification in Patients With Dilated Cardiomyopathy

Background:In patients with dilated (idiopathic) cardiomyopathy (DCM), little is known about the presence of valvular calcification and its association with hypovitaminosis D, which may predispose affected tissues to calcification. Our objectives were 2-fold: to conduct a retrospective assessment of echocardiographic evidence of valvular calcification in patients with DCM who were known to have hypovitaminosis D (25(OH)D <30 ng/mL) and to conduct a prospective assessment of serum 25(OH)D in patients with DCM, who had demonstrated echocardiographic evidence of valvular calcification. Methods:The retrospective study consisted of 48 African American patients (34 men, 14 women; 52.3 ± 1.5 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and 25(OH)D <30 ng/mL; and 20 white patients in the prospective study (20 men; 71.0 ± 3.0 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and echocardiographic evidence of valvular calcification. In the retrospective study, a transthoracic echocardiogram was obtained to address mitral valvular and annular calcification, aortic valvular calcification, and sinotubular calcification; whereas in the prospective study, serum 25(OH)D level was monitored in patients with known valvular calcification. Serum parathyroid hormone (PTH) was monitored in both studies. Results:In the retrospective study, hypovitaminosis D was found in 19 patients (31%) with valvular calcification and in whom serum PTH was increased (83 ± 8 pg/mL). In the prospective study, 15 of 20 elderly patients (80%) with known DCM and valvular calcification were found to have hypovitaminosis D (25(OH)D <30 ng/mL), whereas serum PTH was normal (43 ± 4 pg/mL). Conclusions:In patients with DCM without marked renal dysfunction, valvular calcification was seen more frequently and associated with hypovitaminosis D, whereas in elderly patients with valvular calcification, hypovitaminosis D is common, suggesting that the duration of vitamin D deficiency may determine the extent of valvular calcification. The role of hypovitaminosis D in the appearance of valvular calcification deserves further study.

Secondary Hyperparathyroidism in Heart Failure

ABSTRACT Secondary hyperparathyroidism (SHPT) is a well‐known pathophysiologic feature of chronic renal failure. In recent years, SHPT has become recognized as a complication of the aldosteronism associated with congestive heart failure and where excretory Ca2+ and Mg2+ wasting results in plasma‐ionized hypocalcemia and hypomagnesemia. Elevations in plasma parathyroid hormone have adverse systemic consequences, including intracellular Ca2+ overloading of myocytes and vascular smooth muscle with the induction of oxidative stress. Herein, we briefly review the presence and adverse outcomes of SHPT in persons with heart failure.

Resolution of complete heart block after revascularization of acute marginal branch of the right coronary artery

A patient presented with typical angina and a non-ST elevation myocardial infarction. Electrocardiogram showed complete heart block, and she was found to have a 90% acute marginal artery stenosis. The block resolved after balloon angioplasty of this artery that does not supply the atrioventricular node. We propose that increased vagal tone due to inferior wall ischemia from acute marginal artery stenosis has elicited the Bezold-Jarisch reflex. This is a likely mechanism for this uncommon etiology of complete heart block.

A Mitochondriocentric Pathway to Cardiomyocyte Necrosis: An Upstream Molecular Mechanism in Myocardial Fibrosis

The pathophysiologic origins of heart failure can be attributed to a pathologic remodeling of myocardium, including necrotic loss of cardiomyocytes and consequent reparative fibrosis. Hypertensive heart disease with concentric left ventricular hypertrophy and fibrosis represents a major etiologic factor accounting for diastolic heart failure. Herein, we focus on molecular mechanisms to the precursor of fibrosis, namely, cardiomyocyte necrosis, whose pathogenic origin resides in a mitochondriocentric signal-transducer–effector pathway. Its major components include intracellular Ca2+ overloading of cytosolic and mitochondrial domains, the induction of oxidative stress by these organelles which overwhelms endogenous antioxidant defenses, and the increased opening potential of the mitochondrial permeability transition pore. Novel cardioprotective strategies aimed at preventing the progressive remodeling of the failing heart should target upstream molecular mechanisms that prevent cardiomyocyte necrosis rather than downstream events involving collagen turnover related to fibrosis.

Image Diagnosis: Rapidly Enlarging Scrotal Hematoma: A Complication of Femoral Access?

CASE PRESENTATION A 69-year-old man with known ischemic cardiomyopathy presented to our Emergency Department with chest pain. He underwent cardiac catheterization via right femoral approach with placement of a drug-eluting stent to his mid left anterior descending artery, and dual antiplatelet therapy with aspirin and clopidogrel was started. Postintervention, the arteriotomy site was sealed using a Mynx (CardinalHealth Inc, Dublin, OH) vascular closure device. No immediate postprocedure complications were noted. Overnight, the patient developed hypotension with penile swelling along with a progressively enlarging scrotal hematoma (Figure 1). No access site swelling or hematoma was evident. A computed tomography scan of the abdomen and pelvis showed soft tissue extending from the pelvis into the scrotum (Figure 2). The patient’s baseline hemoglobin level before the procedure was 10.5 g/dL, and hematocrit was 32.2%. At the time the swelling was noted, the patient’s hemoglobin had dropped to 7.5 g/dL, and hematocrit was down to 23.3%. He required transfusion of 2 units of packed red blood cells. The next morning, because of a continued drop in hemoglobin and worsening scrotal swelling, the patient was taken urgently to the catheterization laboratory for right femoral angiography via left femoral approach. The femoral angiogram showed continued spurting of blood from the right common femoral artery access site (Figure 3), probably because of posterior wall puncture during cardiac catheterization. Percutaneous balloon angioplasty was performed using an 8 mm x 40 mm compliant balloon with prolonged inflation (more than 5 minutes) to tamponade the site of the posterior ooze. A subsequent angiogram showed no evidence of bleeding from the common femoral artery (Figure 4). An orthogonal-view angiogram was repeated a few minutes later with similar results. During the next day, the patient’s hemodynamic and hematologic parameters stabilized. There was gradual reduction in the scrotal swelling until complete resolution was confirmed at follow-up 2 weeks later.

Magnesium and Its Interdependency with Other Cations in Acute and Chronic Stressor States

Mg2+ and Ca2+ are major divalent intracellular cations. Mg2+ is integral to a myriad of enzymatic reactions and physiologic responses, especially in tissues such as the heart, where metabolic activity and ATP consumption are high [1]. In addition, there are intricate interdependencies between Mg2+ and Ca2+ and other cations. Numerous examples of the interplay that exists between Mg2+, Ca2+, and K+ have been well recognized. Herein, we focus specifically on several inseparable interconnections involving Mg2+ and those cations which are clinically relevant to the heart during acute and chronic stressor states, wherein neurohormonal activation involving the adrenergic and renin-angiotensin-aldosterone systems unmasks their interdependency.