Hemodynamic effects of inhaled nitric oxide in women with mitral stenosis and pulmonary hypertension

Mahoney, Paul; Loh, Evan; Blitz, Lawrence R.; Herrmann, Howard C.

doi:10.1016/s0002-9149(00)01314-x

Cited by 36 publications

(19 citation statements)

References 18 publications

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“…470 -473 In patients with significant right heart failure after catheter-based or surgical relief of MV obstruction, inhaled nitric oxide, intravenous prostacyclin, or an endothelin antagonist may be useful in reducing pulmonary vascular resistance and pulmonary hypertension. 474 Gradual regression of pulmonary hypertension over months has been demonstrated. 470 -472 Recurrent symptoms after successful surgical commissurotomy have been reported to occur in as many as 60% of patients after 9 years 405,435,475 ; however, recurrent stenosis accounts for symptoms in fewer than 20% of patients.…”

Section: Management Of Patients After Valvotomy or Commissurotomymentioning

confidence: 97%

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

Bonow¹,

Carabello²,

Chatterjee³

et al. 2008

Circulation

910

259

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Section: Management Of Patients After Valvotomy or Commissurotomymentioning

confidence: 97%

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

Bonow¹,

Carabello²,

Chatterjee³

et al. 2008

Circulation

910

259

View full text Add to dashboard Cite

“…Patients with pulmonary venous hypertension have elevated pulmonary venous pressure (as reflected in the pulmonary capillary wedge pressure), most frequently as a consequence of either mitral valve disease 5 or left ventricular (LV) diastolic dysfunction. 6 Although mitral stenosis was the most common cause of this entity decades ago, LV diastolic dysfunction is the most common cause of pulmonary venous hypertension seen in our referral practice.…”

Section: Category 2: Pulmonary Venous Hypertensionmentioning

confidence: 99%

Diagnosis and Treatment of Secondary (Non–Category 1) Pulmonary Hypertension

Rich

Rabinovitch

2008

Circulation

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P ulmonary hypertension occurs commonly in cardiopulmonary disease. In 1998, a new clinical classification was proposed that divided pulmonary hypertension into 5 categories on the basis of the presumed underlying etiology of the pulmonary vascular disease 1 (Table 1). Although it was never intended that this classification be used as a guideline to determine appropriate therapy, somewhat surprisingly, the regulatory authorities decided that all medications that were clinically tested and approved for patients with idiopathic pulmonary arterial hypertension (PAH) and patients with pulmonary hypertension associated with connective tissue diseases be applied to all category 1 patients. 2 The wisdom of this can be debated at a later date. However, it has left clinicians somewhat confused about the utilization of therapies to treat patients who fall outside of category 1 pulmonary hypertension, often referred to as secondary pulmonary hypertension.There are 3 classes of approved therapies for PAH, all of which are considered to be pulmonary vasodilators: endothelin receptor blockers, phosphodiesterase-5 inhibitors, and prostacyclins. 3 Their clinical efficacy has been based on a short-term improvement in exercise tolerance, as measured by a 6-minute walk test. In all of the clinical trials, an improvement in walk was apparent within the first 4 weeks of use, allowing a judgment about efficacy to be made quickly. 4 Hemodynamically, their effects are modest, but they tend to raise cardiac output with little effect on pulmonary artery pressure. This has important implications when they are considered for unapproved use. We review the distinctive features of these causes of pulmonary hypertension and the data on the evidence that supports or refutes the use of these therapies in noncategory 1 pulmonary hypertension. Category 2: Pulmonary Venous HypertensionPatients with pulmonary venous hypertension have elevated pulmonary venous pressure (as reflected in the pulmonary capillary wedge pressure), most frequently as a consequence of either mitral valve disease 5 or left ventricular (LV) diastolic dysfunction. 6 Although mitral stenosis was the most common cause of this entity decades ago, LV diastolic dysfunction is the most common cause of pulmonary venous hypertension seen in our referral practice. 7 It is presumed that the mechanism of both is similar. Specifically, a chronic elevation in the diastolic filling pressure of the left heart causes a backward transmission of the pressure to the pulmonary venous system, which triggers vasoconstriction in the pulmonary arterial bed. 8 Histologically, abnormal thickening of the veins and formation of a neointima are seen. 9 The latter can be quite extensive ( Figure 1). As secondary features, medial hypertrophy and, with time, thickening of the neointima on the arterial side of the pulmonary circulation occur as well. There is great potential for reversibility of these changes with improvement in the cause of the venous hypertension (see below). The variability in the response...

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“…Recent reports suggest that the response of pulmonary artery pressure to inhalation of nitric oxide during cardiac catheterization can be useful to divorce fixed from reversible pulmonary hypertension. 21 …”

Section: Laboratory Diagnosismentioning

confidence: 99%