Management of hypertension in liver transplant patients.

Hypertension is a common co-morbidity and a frequent complication in liver transplant patients. The aim of this paper is to concisely review available clinical data and propose a hypertension treatment algorithm in liver transplant patients. Calcium channel blockers are mainstay of the treatment due to their potent vasodilatory effects. Dihydropyridine calcium channel blockers are preferable due to their least interaction with cytochrome P450 enzyme system and, therefore, minimal risk of potential disruption of immunosuppressive drug levels. Beta-blockers may be considered first line drugs in patients with resting tachycardia and in those with high cardiac outputs. Data support the use of beta-blockers for patients intolerant or unresponsive to calcium channel blockers. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers have little value when used early after liver transplant but may have a more pronounced role during the later periods. Diuretics may be of value in combination with other drugs, especially to counteract the potassium-retaining effects of calcineurin inhibitors. Treatment of post liver transplantation hypertension in patients with co-morbid conditions such as coronary artery disease, diabetes mellitus, congestive heart failure, and renal disease will likely require combination therapy.

Carotid body tumor.

Carotid body tumors are the most common paragangliomas of head and neck. Most of these tumors are benign with a small malignant potential. Although newer non-invasive diagnostic modalities have significantly enhanced the diagnostic capabilities, controversy exists over adequate management of these rare tumors. In younger, healthy patients with no comorbidities, the best therapeutic strategy is a complete excision of the tumor. However, in less than ideal patient population modalities such as radiation and tumor embolization can be considered. Surgical advances have greatly decreased the mortality rates, but the morbidity rates secondary to cranial nerve injuries remain high.

Takotsubo cardiomyopathy as a potential cause of long QT syndrome and torsades de pointes.

Takotsubo cardiomyopathy is an increasingly reported syndrome characterized by transient apical left ventricular dysfunction in absence of flow limiting coronary artery disease. Prolongation of QT interval associated with Takotsubo cardiomyopathy has been previously reported in published case series but none of these series reported occurrence of torsades de pointes. Reported here is a case of Takotsubo cardiomyopathy resulting in QT prolongation and torsades de pointes in an emotionally distressed woman. The patient had a complete recovery of cardiac function in a week. Takotsubo cardiomyopathy should be considered among the causes of long QT syndrome and torsades de pointes.

Lyme carditis: sequential electrocardiographic changes in response to antibiotic therapy.

Lyme disease is a tick-borne spirochetal infection that may involve heart. The cardiac manifestations of Lyme disease including varying degrees of atrioventricular heart block occur within weeks to months of the infecting tick bite. This report describes a 43 year-old man with Lyme carditis who presented with complete heart block. The heart block resolved with ceftriaxone therapy. Lyme carditis should be considered in the differential diagnosis in patients who present with new onset advanced heart block.

Acute stress-induced cardiomyopathy: a brief observation.

Acute stress-induced cardiomyopathy is a syndrome originally described in Japan but increasingly recognized all over the world. Patients typically present with chest pain triggered by an intense emotional or physiological stressor, electrocardiographic changes, and mild cardiac enzyme elevation. Patients typically return to normal cardiac function within 1 month. A retrospective review was conducted of all acute stress-induced cardiomyopathy cases at the University of Maryland Medical Center between May 2006 and May 2007. Six patients fulfilled the criteria and were included in the study. The main clinical features of the syndrome were statistically analyzed. Most patients were post-menopausal women presenting with chest pain. An emotional or physiological stressor was identified in 3 of the 6 patients. Electrocardiographic changes (ST segment elevation or T wave inversion) were present in 3 patients. All patients had left ventricular apical hypokinesis with basal hyperkinesis and elevated cardiac enzymes. The 3 patients receiving a follow up echocardiogram had improved left ventricular contractility and reduced mitral regurgitation within 1 month. Two of the patients had complete resolution in 3-4 days. Stress-induced cardiomyopathy is an important syndrome which mimics an acute myocardial infarction. It is typically self-limiting but can result in ventricular arrhythmias and cardiogenic shock. Our findings should caution clinicians that an identifiable stressor and electrocardiographic changes are not always present. In addition, our observation suggests that patients may regain normal cardiac function in less than 4 days.

CT angiography images of an anomalous right coronary artery.

We describe a 33-year-old male with angina pectoris who was found to have abnormal origin and course of right coronary artery from left aortic cusp. The abnormal origin was identified by conventional coronary angiography but the abnormal course of the vessel between ascending aorta and the main pulmonary artery was precisely delineated by high resolution CT angiography. Patient underwent successful surgical transposition of the anomalous vessel with complete resolution of symptoms.

Cardiac troponin I in sickle cell crisis.

Gross and microscopic findings consistent with acute and healed myocardial injury without coronary artery disease have been described in autopsy studies of patients with sickle cell crisis. The present study was designed to determine whether serum levels of cardiac troponin I are elevated in sickle cell crisis. Cardiac troponin I levels were measured in 32 patients age>18 years with the admission diagnosis of sickle cell crisis. All patients had cardiac troponin I level drawn >24 h after the onset of symptoms. The clinical profile and electrocardiograms were analyzed. Out of 32 patients, 2 patients had serum cardiac troponin I elevated, both had presented with acute chest syndrome. Serum cardiac troponin I may be elevated during sickle cell crisis, possibly by myocardial ischemia resulting from microvascular coronary obstruction during sickle cell crisis.

Does beta blocker therapy affect the diagnostic accuracy of adenosine single-photon-emission computed tomographic myocardial perfusion imaging?

We retrospectively evaluated perfusion defect presence, extent, and severity in 158 consecutive patients receiving beta blockers, who underwent adenosine single-photon-emission computed tomography (SPECT) myocardial perfusion imaging (MPI) and coronary angiography. Seventy-six patients (group 1) had their beta blockers withdrawn 48 hours prior to testing, and 82 patients (group 2) remained on the beta blocker regimen. Groups 1 and 2 were similar in gender, age, pretest symptoms, and history of coronary artery disease (CAD). Group 1 patients had higher resting heart rates (79 +/- 19/min versus 68 +/- 13/min; P < 0.001), peak heart rates (91 +/- 21/min versus 80 +/- 15/min; P < 0.001), resting diastolic blood pressures (82 +/- 14 mm Hg versus 74 +/- 13 mm Hg; P < 0.001), peak systolic blood pressures (139 +/- 23 mm Hg versus 124 +/- 23 mm Hg; P < 0.001), and peak diastolic blood pressures (72 +/- 12 mm Hg versus 68 +/- 11 mm Hg; P = 0.04) than group 2 patients. Group 1 also had a higher incidence of angina during the 48 hours off beta blockers than group 2 (10% versus 2%; P < 0.001). There was no significant difference between the two groups in symptoms and side effects during adenosine infusion, quantitated lung/heart ratio, visually assessed lung uptake, transient ischemic dilation, post-stress ejection fraction, summed stress score, summed rest score, and summed difference score. In conclusion, in patients with CAD, beta blocker therapy does not affect the extent, severity, and reversibility of perfusion defects on adenosine SPECT MPI.

Secondary hypertension: current diagnosis and treatment.

Secondary hypertension affects a small but significant number of the hypertensive population and, unlike primary hypertension, is a potentially curable condition. The determinant for workup is dependent on the index of suspicion elicited during patient examination and treatment. Specific testing is available and must be balanced depending on the risk and cost of the workup and treatment with the benefits obtained if the secondary cause is eliminated. This article reviews common manifestations, workup, and the current treatments of the common causes of secondary hypertension.

Cardiogenic shock: basics and clinical considerations.

Cardiogenic shock is a state of tissue hypoperfusion induced by heart failure after correction of preload. There are no clear numerical cutoffs to define of the hemodynamic parameters of cardiogenic shock but it is usually characterized by low blood pressure (systolic blood pressure <90 mmHg or a drop in mean blood pressure >30 mmHg, both with a heart rate >60 bpm) with low urine output (<0.5 ml/kg/h), with or without evidence of organ congestion. Acute myocardial infarction is the most common cause. Mortality is high but intra-aortic balloon counterpulsation and early coronary interventions have improved the outcome. Activation of inflammatory response resulting in expression of inducible nitric oxide synthase, activation of inflammatory cytokines, and activation of complement system appear to play an important role in the pathogenesis and outcome of cardiogenic shock. Nitric oxide synthase inhibitors and C5 complement inhibitors are being investigated as potentially useful agents for the treatment of cardiogenic shock. Historical perspective, epidemiology, etiology, pathophysiology, risk predictors, and management of cardiogenic shock are described in this review.

Noninvasive imaging of anomalous coronary arteries.

Anomalous coronary arteries are a rare but recognized cause of myocardial ischemia and sudden death. Most patients with coronary anomalies remain asymptomatic because the anomaly either does not produce any symptoms during life or the first manifestation is sudden death. Noninvasive imaging plays crucial role in diagnosis of the potentially life threatening coronary anomalies.

Prosthetic heart valves: types and echocardiographic evaluation.

In the last five decades multiple different models of prosthetic valves have been developed. The purpose of this article is to provide a comprehensive source of information for the types and the echocardiographic evaluation of the prosthetic heart valves.

Fibrosing mediastinitis presenting as pulmonary stenosis: stenting works.

A rare case of fibrosing mediastinitis from histoplasmosis with extrinsic compression of the right pulmonary artery is reported. A 41-year-old patient presented with worsening symptoms of cough, fever, migratory arthralgia, chest pain, and progressive dyspnea. The pulmonary artery involvement was suspected by transthoracic echo and was confirmed by transesophageal echo, CT scan of chest, and right heart catheterization. Diagnosis of histoplasmosis was confirmed by biopsy and serological tests. Patient has been free from symptoms of pulmonary stenosis for 4 years after successful pulmonary artery stenting.

Benazepril induced isolated visceral angioedema: a rare and under diagnosed adverse effect of angiotensin converting enzyme inhibitors.

Angiotensin converting enzyme inhibitors are one of the most commonly prescribed medications and angioedema of upper aerogastric tracts is a well recognized complication. Isolated visceral angioedema with the use of angiotensin converting enzyme inhibitors is rare and is relatively under diagnosed. The visceral angioedema should be considered in patients taking angiotensin converting enzyme inhibitors who develop gastrointestinal complaints. We report a case of subacute intestinal obstruction from the use of benazepril, which was promptly resolved after withdrawing benazepril.

Candida parapsilosis endocarditis 8 months after transient candidemia.

We report a case of aortic valve endocarditis with aortic root abscess from Candida parapsilosis occurring 8 months after transient candidemia. Despite the fact that the patient was treated appropriately, candidemia persisted and later on presented with an embolic stroke as a complication of fungal endocarditis.

Electrocardiographic changes in combined electrolyte depletion.

Cardiac action potential is affected by extracellular gradients in potassium, calcium, and magnesium with resultant electrocardiographic changes varying from subtle findings to marked repolarization abnormalities. This report presents marked electrocardiographic changes resulting from a combination of electrolytes depletion in a patient with bulimia and anorexia nervosa.

Pregnancy-associated plasma protein-A: an emerging cardiac biomarker.

Pregnancy associated plasma protein-A (PAPP-A), originally discovered as a glycoprotein found in the serum of pregnant women, is emerging as a potential biomarker of plaque instability. It is produced by the syncytiotrophoblasts of the placenta and circulates in the form of an approximately 500 kDa heterotetramer. In addition, PAPP-A is present in the sera of men and non-pregnant women at much lower levels in the form of a homodimer, and is produced by a number of different non-placental cell types, including fibroblasts, vascular endothelial cells, and vascular smooth muscle cells. The identification of PAPP-A as a member of the metzincin metalloproteinase superfamily, its synthesis by cell types involved in atherogenesis, and its role in insulin-like growth factor-I regulation has led to the hypothesis that PAPP-A is involved in atherosclerotic plaque progression and instability. Serum PAPP-A may be a biomarker for the detection of vulnerable, unstable plaque. Although early reports appear to validate this hypothesis, adoption of PAPP-A as a clinical cardiac biomarker will need assay standardization and further clinical validation. The clinical validation will require a large and diverse patient population, a clearly defined and uniform diagnostic strategy, incorporation of multiple biomarkers in addition to PAPP-A, and measurement of outcomes data.

Clinical aspects of the Chagas' heart disease.

Chagas' heart disease, caused by protozoan Trypanosoma cruzi, is a common cause of cardiomyopathy in the Americas. Transmission of T. cruzi occurs through Reduviids, the kissing bugs. Less common ways of transmission are blood transfusion, congenital transmission, organ transplantation, laboratory accident, breastfeeding, and oral contamination. Infestation results in cardiac dysautonomia, myocardial apoptosis, and myocardial fibrosis. In acute phase, death is mostly caused by myocarditis and in chronic phase, it is mostly by irreversible cardiomyopathy. A majority of the patients with Chagas' disease remain in the latent phase of disease for 10 to 30 years or even for life. Specific anti-Chagas' therapy with trypanocide drugs is useful in acute phase but the management of chronic Chagas' heart disease is mostly empirical. The mortality during the acute phase of cardiac Chagas is around 5%. Five-year mortality of chronic Chagas' disease with cardiac dysfunction is above 50%. The clinical aspects of the Chagas' heart disease are concisely reviewed.

Cardiac troponin I release in non-ischemic reversible myocardial injury from parvovirus B19 myocarditis.

Cardiac troponin I is released from myocytes in both reversible and irreversible myocardial injury. The changes in myocyte membrane permeability resulting from the injury could be enough for the release of cardiac troponins from the free cytosolic pool of myocytes without structural damage. We report a case of parvovirus B19 myocarditis in a 26-year-old male who developed regional wall motion abnormalities and severe left ventricular systolic dysfunction with elevated serum levels of cardiac troponin I (peak=11.7 ng/ml). Diagnosis of parvovirus myocarditis was confirmed by presence of high titers of parvovirus B19 IgG and identification of parvovirus B19 DNA by polymerase chain reaction. Within a few days of supportive treatment, the regional wall motion abnormalities resolved, the cardiac function recovered, and the elevation in serum cardiac troponin I subsided. This case further denotes the possibility of release of cardiac troponin I in non-ischemic, reversible myocardial injury.