A 31-year-old woman was admitted in a state of cardiogenic shock 6 months after she was diagnosed with nonischemic cardiomyopathy. Nearly 9 to 12 months ago, she had started experiencing fatigue and dyspnea while climbing stairs and was diagnosed with left ventricular systolic dysfunction a few months later. She had ejection fraction of 15% and dilated left ventricle of 6.8 cm and was started on medicines and evidence-based treatment. More recently, she developed intolerance toward her current carvedilol dose that had to be reduced as it caused hypotension and nausea. Currently, the patient was admitted with blood pressure of 88/62 mm Hg, heart rate of 105 beats per minute, S3 gallop on examination, elevated jugular venous distention to 6 cm above the clavicle, cool extremities, brain natriuretic peptide of 953 pg/mL, serum sodium of 134 mmol/L, and total bilirubin of 4 mg/dL. The physician started her on an inotrope upon admission. After diuresis, her right heart catheterization revealed elevated filling pressures (right atrial pressure of 15 mm Hg, wedge pressure of 36 mm Hg), pulmonary hypertension (mean pulmonary artery pressure of 49 mm Hg), and low cardiac index <1.8 on dobutamine 5 μg/kg/min. Echo now revealed progression of left ventricular dilation to 7.2 cm, moderate mitral regurgitation, and moderate right ventricular dysfunction in addition to left-sided failure. Due to advanced stage of the disease and clinical decline in patient's condition, she was worked up for cardiac transplantation and listed with blood type O. Meanwhile, she continued to decline requiring 2 inotropes, and a repeat hemodynamic evaluation showed a high pulmonary vascular resistance of 4.5 Wood units. Her chances of receiving a cardiac transplant were also limited by both her blood type (type O) and worsening pulmonary hypertension. Besides, she could not tolerate attempts to wean her off the inotrope or pressor support, and continued to become more tachycardic. So a decision was made to implant ventricular assist device that would act as a bridge to cardiac transplantation by extending the life of the patient.
Heart failure is a complex clinical syndrome with increasing prevalence and incidence in developed and developing nations. Among adults in the United States, heart failure is now the leading etiology for inpatient admissions. Women represent half of these hospital admissions and heart failure accounts for approximately one-third of all deaths from cardiovascular disease in women.1,2,3 Although women bear a significant burden of heart failure mortality and morbidity, they are historically very poorly represented in clinical trials: prior to 2002, only one-fifth of patients enrolled in randomized controlled trials were women.4 Therefore a paucity of evidence exists regarding gender-specific differences in the diagnosis, treatment, and prognosis of heart failure.
Recent analysis revealed differential autosomal gene expression in men versus women with heart failure.5,6,7 Women overexpressed genes related to adrenergic and angiotensin signaling, cyclic nucleotide metabolism, and glucose transport (GATAD1, PDE6B, and SCLA12, respectively). Those genes upregulated in men with heart failure were associated with potassium channel/arrhythmia regulation, cellular homeostasis, and immune system regulation (KCNK1, PLEKHA8, and CD24, respectively). These initial genetic studies may provide an early foundation to explain the gender differences noted in etiology (eg, ischemic vs nonischemic secondary to hypertensive heart disease), presentation (eg, with age differences), clinical course, and response to treatment in heart failure—or personalized medicine based on sex-related heart failure management.
The prevalence of heart failure increases in both men and women as the population ages. However, the initial diagnosis of heart failure occurs later in women, and more women than men have heart failure after the age of 80.8 The most recent ...