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<article article-type="case-report" dtd-version="1.1" specific-use="sps-1.9" xml:lang="en" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">
	<front>
		<journal-meta>
			<journal-id journal-id-type="publisher-id">ABC HF</journal-id>
			<journal-title-group>
				<journal-title>ABC: Heart Failure &amp; Cardiomyopathy</journal-title>
				<abbrev-journal-title abbrev-type="publisher">ABC Heart Fail Cardiomyop</abbrev-journal-title>
			</journal-title-group>
			<issn pub-type="epub">2764-3107</issn>
			<publisher>
				<publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
			</publisher>
		</journal-meta>
		<article-meta>
			<article-id pub-id-type="publisher-id">abchf.20220048</article-id>
			<article-id pub-id-type="doi">10.36660/abchf.20220048</article-id>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Case Report</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Management of Patients with Advanced Heart Failure According to Hemodynamic Parameters</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-1512-5899</contrib-id>
					<name>
						<surname>Aragão</surname>
						<given-names>Carlos Aurélio dos Santos</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<name>
						<surname>Dan</surname>
						<given-names>Daniella Motta da Costa</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<name>
						<surname>Ávila</surname>
						<given-names>Mônica Samuel</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"><sup>1</sup></xref>
					<xref ref-type="corresp" rid="c1"/>
				</contrib>
				<aff id="aff1">
					<label>1</label>
					<institution content-type="orgname">Universidade de São Paulo</institution>
					<institution content-type="orgdiv1">Faculdade de Medicina</institution>
					<institution content-type="orgdiv2">Hospital das Clínicas</institution>
					<addr-line>
						<named-content content-type="city">São Paulo</named-content>
						<named-content content-type="state">SP</named-content>
					</addr-line>
					<country country="BR">Brazil</country>
					<institution content-type="original">Instituto do Coração (InCor), Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP – Brazil</institution>
				</aff>
			</contrib-group>
			<author-notes>
				<corresp id="c1"><bold>Mailing Address: Monica Samuel Avila</bold> • Rua Dr. Enéas de Carvalho Aguiar, 44. Postal Code <postal-code>05403-900</postal-code>, São Paulo, SP – Brazil, E-mail: <email>mo_avila@hotmail.com</email>
				</corresp>
				<fn fn-type="con">
					<p><bold>Author Contributions</bold></p>
					<p>Conception and design of the research, Acquisition of data, Analysis and interpretation of the data, Statistical analysis, Writing of the manuscript and Critical revision of the manuscript for intellectual content: Aragão CAS, Costa DM, Ávila MS.</p>
				</fn>
				<fn fn-type="conflict">
					<p><bold>Potential Conflict of Interest</bold></p>
					<p>No potential conflict of interest relevant to this article was reported.</p>
				</fn>
			</author-notes>
			<pub-date date-type="pub" publication-format="electronic">
				<day>29</day>
				<month>06</month>
				<year>2022</year>
			</pub-date>
			<pub-date date-type="collection" publication-format="electronic">
				<season>Apr-Jun</season>
				<year>2022</year>
			</pub-date>
			<volume>2</volume>
			<issue>2</issue>
			<fpage>234</fpage>
			<lpage>236</lpage>
			<history>
				<date date-type="received">
					<day>28</day>
					<month>03</month>
					<year>2022</year>
				</date>
				<date date-type="rev-recd">
					<day>18</day>
					<month>04</month>
					<year>2022</year>
				</date>
				<date date-type="accepted">
					<day>03</day>
					<month>05</month>
					<year>2022</year>
				</date>
			</history>
			<permissions>
				<license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
					<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License</license-p>
				</license>
			</permissions>
			<kwd-group xml:lang="en">
				<title>Keywords</title>
				<kwd>Management</kwd>
				<kwd>Advanced Heart Failure</kwd>
				<kwd>Hemodynamics</kwd>
			</kwd-group>
			<counts>
				<fig-count count="0"/>
				<table-count count="4"/>
				<equation-count count="0"/>
				<ref-count count="10"/>
				<page-count count="3"/>
			</counts>
		</article-meta>
	</front>
	<body>
		<sec sec-type="intro">
			<title>Introduction</title>
			<p>Heart failure (HF) is characterized by progressive functional or structural worsening of the myocardium. Despite significant therapeutic advances that have improved survival and quality of life, HF still has high morbidity and mortality rates. Patients with HF may progress with refractory disease, whose gold standard treatment is heart transplantation (HT).<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup></p>
			<p>The assessment of pulmonary hemodynamics is indicated for HT candidates. The presence of fixed pulmonary hypertension (PH) is a contraindication for HT because it promotes right ventricular (RV) dysfunction in the graft, reducing post-HT survival. In addition, the assessment of hemodynamic parameters helps in bedside therapeutic management, including in the setting of PH, favoring HT indication.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> We report a successful case of optimal bedside therapy guided by invasive hemodynamic parameters.</p>
		</sec>
		<sec sec-type="cases">
			<title>Case report</title>
			<p>A 58-year-old man with diabetes, stage D HF secondary to idiopathic dilated cardiomyopathy, and recurrent hospitalizations despite optimal drug therapy was referred for outpatient HT evaluation, with evidence of reversible PH after vasodilator testing (<xref ref-type="table" rid="t1">Table 1</xref>). The patient required hospitalization due to disease progression, pulmonary congestion, and peripheral hypoperfusion. Echocardiogram showed a left ventricular ejection fraction of 25% with diffuse hypokinesia, left ventricular (LV) diastolic and systolic diameters of 68 x 64 mm, moderate RV hypokinesia (S’ wave 6 cm/s; TAPSE 26 mm), and a pulmonary artery systolic pressure (PASP) of 55 mm Hg, with severe tricuspid regurgitation. Due to clinical severity, the patient was started on intravenous inotropic, diuretic, and vasodilator support. The patient underwent a new hemodynamic assessment with the use of a pulmonary artery catheter (PAC) in an intensive care setting, with evidence of PH (<xref ref-type="table" rid="t2">Table 2</xref>). Since the patient’s clinical condition was a contraindication for HT, the implant of a long-term ventricular assist device (VAD) was considered but not conducted due to social reasons. The patient was placed on the HT waiting list for heterotopic transplantation, and therapeutic support was optimized with a combination of milrinone, circulatory support via intra-aortic balloon pumping (IABP), and inhaled nitric oxide.</p>
			<table-wrap id="t1">
				<label>Table 1</label>
				<caption>
					<title>Right heart catheterization before hospitalization</title>
				</caption>
				<table frame="hsides" rules="rows">
					<colgroup width="33%">
						<col/>
						<col/>
						<col/>
					</colgroup>
					<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
						<tr>
							<th align="center" valign="middle"/>
							<th align="center" valign="middle">Before vasodilator testing</th>
							<th align="center" valign="middle">After vasodilator testing</th>
						</tr>
					</thead>
					<tbody style="border-bottom: thin solid; border-color: #000000">
						<tr>
							<td align="left" valign="middle">CO</td>
							<td align="center" valign="middle">2.8 L/min</td>
							<td align="center" valign="middle">2.8 L/min</td>
						</tr>
						<tr>
							<td align="left" valign="middle">CVP</td>
							<td align="center" valign="middle">12 mm Hg</td>
							<td align="center" valign="middle">5 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PBP</td>
							<td align="center" valign="middle">74 x 30 mm Hg</td>
							<td align="center" valign="middle">26 x 11 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">mPBP</td>
							<td align="center" valign="middle">44 mm Hg</td>
							<td align="center" valign="middle">17 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PCWP</td>
							<td align="center" valign="middle">25 mm Hg</td>
							<td align="center" valign="middle">5 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">TPG</td>
							<td align="center" valign="middle">19</td>
							<td align="center" valign="middle">12</td>
						</tr>
						<tr>
							<td align="left" valign="middle">DPG</td>
							<td align="center" valign="middle">5 mm Hg</td>
							<td align="center" valign="middle">6 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PVR</td>
							<td align="center" valign="middle">6.7 Wood</td>
							<td align="center" valign="middle">4.2 Wood</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PAPP</td>
							<td align="center" valign="middle">44 mm Hg</td>
							<td align="center" valign="middle">15 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PAPi</td>
							<td align="center" valign="middle">3.6</td>
							<td align="center" valign="middle">3.0</td>
						</tr>
					</tbody>
				</table>
				<table-wrap-foot>
					<fn id="TFN1">
						<p><italic>CO: cardiac output; CVP: central venous pressure; DPG: diastolic pulmonary gradient; mPBP: mean pulmonary blood pressure; PAPi: pulmonary artery pulsatility index; PAPP: pulmonary arterial pulse pressure; PBP: pulmonary blood pressure – diastolic and systolic; PCWP: pulmonary capillary wedge pressure; PVR: pulmonary vascular resistance; TPG: transpulmonary pressure gradient.</italic></p>
					</fn>
				</table-wrap-foot>
			</table-wrap>
			<table-wrap id="t2">
				<label>Table 2</label>
				<caption>
					<title>Progression of hemodynamic parameters during hospitalization and after 4 months of optimal guided therapy</title>
				</caption>
				<table frame="hsides" rules="rows">
					<colgroup width="33%">
						<col/>
						<col/>
						<col/>
					</colgroup>
					<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
						<tr>
							<th align="center" valign="middle"/>
							<th align="center" valign="middle">During hospitalization</th>
							<th align="center" valign="middle">After 4 months</th>
						</tr>
					</thead>
					<tbody style="border-bottom: thin solid; border-color: #000000">
						<tr>
							<td align="left" valign="middle">CO</td>
							<td align="center" valign="middle">5.4 L/min</td>
							<td align="center" valign="middle">6.6 L/min</td>
						</tr>
						<tr>
							<td align="left" valign="middle">CVP</td>
							<td align="center" valign="middle">5 mm Hg</td>
							<td align="center" valign="middle">21 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PBP</td>
							<td align="center" valign="middle">50 x 22 mm Hg</td>
							<td align="center" valign="middle">58 x 33 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">mPBP</td>
							<td align="center" valign="middle">30 mm Hg</td>
							<td align="center" valign="middle">41 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PCWP</td>
							<td align="center" valign="middle">9 mm Hg</td>
							<td align="center" valign="middle">32 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">TPG</td>
							<td align="center" valign="middle">21</td>
							<td align="center" valign="middle">9</td>
						</tr>
						<tr>
							<td align="left" valign="middle">DPG</td>
							<td align="center" valign="middle">13 mm Hg</td>
							<td align="center" valign="middle">1 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PVR</td>
							<td align="center" valign="middle">3.8 Wood</td>
							<td align="center" valign="middle">1.3 Wood</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PAPP</td>
							<td align="center" valign="middle">28 mm Hg</td>
							<td align="center" valign="middle">25 mm Hg</td>
						</tr>
						<tr>
							<td align="left" valign="middle">PAPi</td>
							<td align="center" valign="middle">5.6</td>
							<td align="center" valign="middle">1.1</td>
						</tr>
					</tbody>
				</table>
				<table-wrap-foot>
					<fn id="TFN2">
						<p><italic>CO: cardiac output; CVP: central venous pressure; DPG: diastolic pulmonary gradient; mPBP: mean pulmonary blood pressure; PAPi: pulmonary artery pulsatility index; PAPP: pulmonary arterial pulse pressure; PBP: pulmonary blood pressure – diastolic and systolic; PCWP: pulmonary capillary wedge pressure; PVR: pulmonary vascular resistance; TPG: transpulmonary pressure gradient.</italic></p>
					</fn>
				</table-wrap-foot>
			</table-wrap>
			<p>After 4 months on the waiting list, a new invasive evaluation with a PAC identified significant reduction in pulmonary pressures (<xref ref-type="table" rid="t2">Table 2</xref>), supporting orthotopic transplantation. The patient underwent an HT 5 months after hospitalization with no complications.</p>
		</sec>
		<sec sec-type="discussion">
			<title>Discussion</title>
			<p>The case reported here illustrates the impact of optimal therapy on the improvement of hemodynamic parameters, assessed by serial invasive evaluation with a PAC, in a patient with decompensated HF and cardiogenic shock. PH associated with heart disease, called postcapillary pulmonary hypertension, is characterized by elevation in filling pressures, mean pulmonary blood pressure (mPBP), and pulmonary capillary wedge pressure (PCWP) and constitutes a marker of disease progression in HF with reduced ejection fraction. PH is characterized by an mPBP &gt; 20 mm Hg and a pulmonary vascular resistance (PVR) ≥ 3 Wood;<sup><xref ref-type="bibr" rid="B3">3</xref>,<xref ref-type="bibr" rid="B4">4</xref></sup> if PCWP &gt; 15 mm Hg, PH is considered postcapillary. In this case, the increase in pulmonary artery pressure occurs by retrograde transmission of increased hydrostatic pressure from the left atrium into the pulmonary veins and capillaries.<sup><xref ref-type="bibr" rid="B5">5</xref></sup></p>
			<p>Elevated central venous pressure resistant to drug therapy may be considered a contraindication for HT. In patients with evidence of PH, testing with intravenous vasodilators should be performed to demonstrate whether PH is reversible. Continuous 24-hour to 48-hour monitoring with full therapy consisting of diuretics, inotropes, and intravenous and inhaled vasodilators should be encouraged in cases of irreversible PH.<sup><xref ref-type="bibr" rid="B6">6</xref></sup></p>
			<p>Long-term VADs are a therapeutic option in patients that cannot undergo an HT as they may promote LV decompression, reduction in filling pressures, and, consequently, reduction in pulmonary pressures.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> VAD indication in Brazil in the setting of public health is limited due to socioeconomic conditions. In this case, heterotopic transplantation may be an option with limited results.</p>
			<p>In heterotopic HT, the graft is connected to the native heart, which is maintained in the patient’s rib cage, and acts as a biological LVAD. This procedure may be considered in patients with obesity or increased PVR. However, the feasibility of the procedure remains uncertain.</p>
			<p>Improvement in LV systolic volume causes increased RV preload, which may result in poor RV performance and compliance. Therefore, the presence of previous RV dysfunction is a contraindication for both VAD implantation and heterotopic HT, which were not good options for our patient.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
			<p>Optimal therapy with parenteral and inhaled vasodilators promoted PASP and PCWP reduction, resulting in a decreased transpulmonary pressure gradient and increased cardiac output by reductions in RV afterload, LV preload, and, consequently, PVR. Hypervolemia reduction, on the other hand, promoted reduction in pulmonary pressures.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Dobutamine acts on the beta-1 adrenergic receptor increasing calcium influx and resulting in myocardial contractility. Milrinone is a phosphodiesterase-3 inhibitor that is involved in cyclic guanosine monophosphate degradation, leading to an increase in calcium influx and inotropism.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> Due to phosphodiesterase inhibition, pulmonary vasodilation with a consequent reduction in PH and optimal RV afterload were observed.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> The mechanism of action of IABP is aortic counterpulsation, aortic root diastolic pressure augmentation, afterload reduction, and, consequently, CO increase.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup></p>
			<p>The use of mechanical circulatory support should be considered in patients with a potentially reversible disease and pharmacologically irreversible PH. According to the International Society for Heart and Lung Transplantation, the use of mechanical circulatory support in the management of patients with HP is a class IIB recommendation.<sup><xref ref-type="bibr" rid="B6">6</xref>.</sup></p>
			<p>The Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) reported adverse events associated with the use of PACs, such as arrhythmias, sepsis, pulmonary artery perforation or rupture, and even death. Therefore, the risks of PACs outweigh the benefits, leading several guidelines to not indicate pulmonary artery catheterization.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> However, if used with caution in combination with risk minimization techniques, PACs could help optimize patient support, as occurred in the case reported here.</p>
		</sec>
		<sec sec-type="conclusions">
			<title>Conclusion</title>
			<p>The advanced stages of HF are challenging from a therapeutic perspective, especially when deciding on the optimal destination therapy. PH is a marker of advanced HF, and the use of invasive monitoring may be useful to optimize bedside therapy and to adjust hemodynamic parameters that allow for HT.</p>
		</sec>
	</body>
	<back>
		<fn-group>
			<fn fn-type="supported-by" id="fn1">
				<p><bold>Sources of Funding</bold></p>
				<p>There were no external funding sources for this study.</p>
			</fn>
			<fn fn-type="other" id="fn2">
				<p><bold>Study Association</bold></p>
				<p>This study is not associated with any thesis or dissertation work.</p>
			</fn>
			<fn fn-type="other" id="fn3">
				<p><bold>Ethics approval and consent to participate</bold></p>
				<p>This article does not contain any studies with human participants or animals performed by any of the authors.</p>
			</fn>
		</fn-group>
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	<sub-article article-type="translation" id="S01" xml:lang="pt">
		<front-stub>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Relato de Caso</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Manejo do Paciente com IC Avançada Baseado em Parâmetros Hemodinâmicos</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0002-1512-5899</contrib-id>
					<name>
						<surname>Aragão</surname>
						<given-names>Carlos Aurélio dos Santos</given-names>
					</name>
					<xref ref-type="aff" rid="aff2"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<name>
						<surname>Dan</surname>
						<given-names>Daniella Motta da Costa</given-names>
					</name>
					<xref ref-type="aff" rid="aff2"><sup>1</sup></xref>
				</contrib>
				<contrib contrib-type="author">
					<name>
						<surname>Ávila</surname>
						<given-names>Mônica Samuel</given-names>
					</name>
					<xref ref-type="aff" rid="aff2"><sup>1</sup></xref>
					<xref ref-type="corresp" rid="c2"/>
				</contrib>
				<aff id="aff2">
					<label>1</label>
					<addr-line>
						<named-content content-type="city">São Paulo</named-content>
						<named-content content-type="state">SP</named-content>
					</addr-line>
					<country country="BR">Brasil</country>
					<institution content-type="original">Instituto do Coração (InCor), Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP – Brasil</institution>
				</aff>
			</contrib-group>
			<author-notes>
				<corresp id="c2"><bold>Correspondência: Monica Samuel Avila</bold> • Rua Dr. Enéas de Carvalho Aguiar, 44. CEP <postal-code>05403-900</postal-code>, São Paulo, SP – Brasil, E-mail: <email>mo_avila@hotmail.com</email>
				</corresp>
				<fn fn-type="con">
					<p><bold>Contribuição dos autores</bold></p>
					<p>Concepção e desenho da pesquisa, Obtenção de dados, Análise e interpretação dos dados, Análise estatística, Redação do manuscrito e Revisão crítica do manuscrito quanto ao conteúdo intelectual importante: Aragão CAS, Costa DM, Ávila MS.</p>
				</fn>
				<fn fn-type="conflict">
					<p><bold>Potencial conflito de interesse</bold></p>
					<p>Não há conflito com o presente artigo</p>
				</fn>
			</author-notes>
			<kwd-group xml:lang="pt">
				<title>Palavras-chave:</title>
				<kwd>Administração dos Cuidados ao Paciente</kwd>
				<kwd>Insuficiência Cardíaca</kwd>
				<kwd>Hemodinâmica</kwd>
			</kwd-group>
		</front-stub>
		<body>
			<sec sec-type="intro">
				<title>Introdução</title>
				<p>A insuficiência cardíaca (IC) é caracterizada pelo declínio progressivo, estrutural e/ou funcional do miocárdio. Apesar do significativo avanço terapêutico e da consequente melhora na sobrevida e qualidade de vida, a IC permanece com altos índices de morbimortalidade. Os pacientes com IC podem evoluir para refratariedade, cujo tratamento padrão-ouro é o transplante cardíaco (TC).<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup></p>
				<p>A avaliação da hemodinâmica pulmonar é indicada para pacientes candidatos a TC, pois a presença de hipertensão arterial pulmonar (HAP) fixa é considerada um critério limitante ao TC, visto que favorece a disfunção de ventrículo direito (VD) no enxerto, reduzindo a sobrevida pós-TC. Além disso, a avaliação dos parâmetros hemodinâmicos auxilia no manejo terapêutico à beira do leito, inclusive em contexto de HAP, a fim de favorecer a indicação ao TC.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> O objetivo do presente estudo foi relatar um desfecho satisfatório pós-otimização terapêutica à beira do leito guiada por parâmetros hemodinâmicos invasivos.</p>
			</sec>
			<sec sec-type="cases">
				<title>Relato de Caso</title>
				<p>Paciente masculino, 58 anos, diabético, portador de IC em estágio D secundária a miocardiopatia dilatada idiopática, com internações recorrentes a despeito da terapia medicamentosa otimizada. Iniciou-se avaliação para TC em nível ambulatorial, com evidência de HAP e reversibilidade após a prova com vasodilatador (<xref ref-type="table" rid="t3">Tabela 1</xref>). O paciente evoluiu com necessidade de internação por progressão de doença, congestão pulmonar e hipoperfusão periférica. O ecocardiograma demonstrou fração de ejeção do ventrículo esquerdo (FEVE) de 25% com hipocinesia difusa, diâmetro diastólico e sistólico do ventrículo esquerdo (VE) de 68 x 64 mm, VD com hipocinesia moderada (onda S de 6 cm/s; excursão sistólica do plano do anel tricúspide [TAPSE] de 26 mm) e pressão sistólica da artéria pulmonar (PSAP) de 55 mmHg, com insuficiência tricúspide importante. Devido à gravidade clínica, foi iniciado suporte inotrópico, diurético e vasodilatador endovenoso. O paciente foi submetido à nova avaliação hemodinâmica com cateter de artéria pulmonar (CAP) em ambiente de terapia intensiva com evidência de HAP (<xref ref-type="table" rid="t4">Tabela 2</xref>). Considerando o cenário clínico como um limitante para o TC, foi aventado o implante de dispositivo de assistência ventricular (DAV) de longa duração, o que não procedeu por questões sociais. Optou-se pela inclusão em fila para transplante cardíaco heterotópico, e foi otimizado suporte terapêutico com associação de milrinona, suporte mecânico com balão intra-aórtico (BIA) e óxido nítrico inalatório.</p>
				<table-wrap id="t3">
					<label>Tabela 1</label>
					<caption>
						<title>Cateterismo cardíaco direito pré-internação hospitalar</title>
					</caption>
					<table frame="hsides" rules="rows">
						<colgroup width="33%">
							<col/>
							<col/>
							<col/>
						</colgroup>
						<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
							<tr>
								<th align="center" valign="middle"/>
								<th align="center" valign="middle">Pré-prova vasodilatadora</th>
								<th align="center" valign="middle">Pós-prova vasodilatadora</th>
							</tr>
						</thead>
						<tbody style="border-bottom: thin solid; border-color: #000000">
							<tr>
								<td align="left" valign="middle">DC</td>
								<td align="center" valign="middle">2,8 L/min</td>
								<td align="center" valign="middle">2,8 L/min</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PVC</td>
								<td align="center" valign="middle">12 mmHg</td>
								<td align="center" valign="middle">5 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PAP</td>
								<td align="center" valign="middle">74 x 30 mmHg</td>
								<td align="center" valign="middle">26 x 11 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PmAP</td>
								<td align="center" valign="middle">44 mmHg</td>
								<td align="center" valign="middle">17 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PCP</td>
								<td align="center" valign="middle">25 mmHg</td>
								<td align="center" valign="middle">5 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">GTP</td>
								<td align="center" valign="middle">19</td>
								<td align="center" valign="middle">12</td>
							</tr>
							<tr>
								<td align="left" valign="middle">GDP</td>
								<td align="center" valign="middle">5 mmHg</td>
								<td align="center" valign="middle">6 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">RVP</td>
								<td align="center" valign="middle">6,7 Woods</td>
								<td align="center" valign="middle">4,2 Woods</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PPAP</td>
								<td align="center" valign="middle">44 mmHg</td>
								<td align="center" valign="middle">15 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PAPi</td>
								<td align="center" valign="middle">3,6</td>
								<td align="center" valign="middle">3,0</td>
							</tr>
						</tbody>
					</table>
					<table-wrap-foot>
						<fn id="TFN3">
							<p><italic>DC: débito cardíaco; PVC: pressão venosa central; PAP: pressão arterial pulmonar – sistólica e diastólica; PmAP: pressão média da artéria pulmonar; PCP: pressão capilar pulmonar; GTP: gradiente transpulmonar; GDP: gradiente diastólico da artéria pulmonar; RVP: resistência vascular pulmonar; PPAP: pressão de pulso da artéria pulmonar; PAPi: índice de pulsatilidade da artéria pulmonar.</italic></p>
						</fn>
					</table-wrap-foot>
				</table-wrap>
				<table-wrap id="t4">
					<label>Tabela 2</label>
					<caption>
						<title>Evolução dos parâmetros hemodinâmicos durante internação e após 4 meses de otimização terapêutica guiada</title>
					</caption>
					<table frame="hsides" rules="rows">
						<colgroup width="33%">
							<col/>
							<col/>
							<col/>
						</colgroup>
						<thead style="border-top: thin solid; border-bottom: thin solid; border-color: #000000">
							<tr>
								<th align="center" valign="middle"/>
								<th align="center" valign="middle">Durante internação</th>
								<th align="center" valign="middle">Após 4 meses</th>
							</tr>
						</thead>
						<tbody style="border-bottom: thin solid; border-color: #000000">
							<tr>
								<td align="left" valign="middle">DC</td>
								<td align="center" valign="middle">5,4 L/min</td>
								<td align="center" valign="middle">6,6 L/min</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PVC</td>
								<td align="center" valign="middle">5 mmHg</td>
								<td align="center" valign="middle">21 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PAP</td>
								<td align="center" valign="middle">50 x 22 mmHg</td>
								<td align="center" valign="middle">58 x 33 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PmAP</td>
								<td align="center" valign="middle">30 mmHg</td>
								<td align="center" valign="middle">41 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PCP</td>
								<td align="center" valign="middle">9 mmHg</td>
								<td align="center" valign="middle">32 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">GTP</td>
								<td align="center" valign="middle">21</td>
								<td align="center" valign="middle">9</td>
							</tr>
							<tr>
								<td align="left" valign="middle">GDP</td>
								<td align="center" valign="middle">13 mmHg</td>
								<td align="center" valign="middle">1 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">RVP</td>
								<td align="center" valign="middle">3,8 Wood</td>
								<td align="center" valign="middle">1,3 Wood</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PPAP</td>
								<td align="center" valign="middle">28 mmHg</td>
								<td align="center" valign="middle">25 mmHg</td>
							</tr>
							<tr>
								<td align="left" valign="middle">PAPi</td>
								<td align="center" valign="middle">5,6</td>
								<td align="center" valign="middle">1,1</td>
							</tr>
						</tbody>
					</table>
					<table-wrap-foot>
						<fn id="TFN4">
							<p><italic>DC: débito cardíaco; PVC: pressão venosa central; PAP: pressão arterial pulmonar – sistólica e diastólica; PmAP: pressão média da artéria pulmonar; PCP: pressão capilar pulmonar; GTP: gradiente transpulmonar; GDP: gradiente diastólico da artéria pulmonar; RVP: resistência vascular pulmonar; PPAP: pressão de pulso da artéria pulmonar; PAPi: índice de pulsatilidade da artéria pulmonar.</italic></p>
						</fn>
					</table-wrap-foot>
				</table-wrap>
				<p>Após 4 meses à espera do transplante heterotópico, foi realizada nova avaliação invasiva com CAP, e observou-se redução significativa das pressões pulmonares (<xref ref-type="table" rid="t4">Tabela 2</xref>), o que é favorável ao transplante ortotópico, o qual foi realizado após 5 meses da internação, sem intercorrências.</p>
			</sec>
			<sec sec-type="discussion">
				<title>Discussão</title>
				<p>O caso relatado ilustra o impacto da otimização terapêutica na melhora dos parâmetros hemodinâmicos de um paciente com IC descompensada e choque cardiogênico, avaliado por medidas invasivas seriadas através do CAP.</p>
				<p>A HAP associada a doenças cardíacas, a hipertensão pulmonar pós-capilar, é caracterizada por elevação das pressões de enchimento, da pressão média da artéria pulmonar (PmAP) e da pressão capilar pulmonar (PCP), e constitui um marcador de progressão de doença na IC com FEVE reduzida. A HAP é definida por PmAP superior a 20 mmHg e resistência vascular pulmonar (RVP) maior ou igual a 3 Wood.<sup><xref ref-type="bibr" rid="B3">3</xref>–<xref ref-type="bibr" rid="B4">4</xref></sup> Quando a PCP for superior a 15 mmHg, a HAP é reconhecidamente pós-capilar. Nesse caso, a elevação da pressão do território arterial pulmonar ocorre por transmissão retrógrada do aumento da pressão hidrostática do átrio esquerdo, para o leito venocapilar pulmonar.<sup><xref ref-type="bibr" rid="B5">5</xref></sup></p>
				<p>A elevação da RVP refratária ao tratamento medicamentoso pode ser considerada uma contraindicação ao TC. Em pacientes com evidência de HAP, deve-se realizar a prova com vasodilatadores endovenosos, com o objetivo de demonstrar a reversibilidade da HAP. Uma monitorização contínua por 24 a 48 horas, com uma terapêutica máxima com diuréticos, inotrópicos, vasodilatadores endovenosos e inalatórios, deve ser encorajada nos casos de HAP irreversível.<sup><xref ref-type="bibr" rid="B6">6</xref></sup></p>
				<p>proibitivas ao TC, mediante a possibilidade de descompressão do VE e queda das pressões de enchimento e consequente queda das pressões pulmonares.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> A indicação dos DAVs no Brasil em contexto de saúde pública é limitada devido às condições socioeconômicas. Nesse panorama, o transplante heterotópico pode ser uma opção com resultados limitados.</p>
				<p>O TC heterotópico tem como base um coração nativo que é mantido na caixa torácica conectado ao coração doado heterotópico, atuando como um dispositivo biológico de assistência ventricular esquerda. Tal procedimento pode ser considerado para obesos e para pacientes com RVP elevada. Todavia, os resultados são incertos quanto à sua viabilidade.</p>
				<p>Mediante a melhora do volume sistólico ventricular esquerdo, há aumento da pré-carga do VD, o que pode piorar a performance e complacência do VD. Por isso, tanto para os DAVs como para o TC heterotópico, a disfunção prévia do VD é proibitiva – ou seja, são opções não favoráveis para o paciente em questão.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
				<p>A otimização da terapia vasodilatadora parenteral e inalatória contribuiu para a redução da PSAP e da PCP, resultando no declínio do gradiente transpulmonar (GTP) e incremento do débito cardíaco (DC) através da redução da pós-carga do VD e da pré-carga do VE e, por conseguinte, da RVP. A redução da hipervolemia, por sua vez, contribuiu para redução das pressões pulmonares.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> A dobutamina age no receptor adrenérgico beta-1 e aumenta o influxo de cálcio, o que resulta em contratilidade miocárdica. Já a milrinona é um inibidor da fosfodiesterase-3, que atua na degradação do monofosfato cíclico de guanosina (GMPc), o que incrementa o influxo de cálcio e inotropismo.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> Devido à inibição da fosfodiesterase, observa-se vasodilatação pulmonar e consequente queda da HAP e otimização da pós-carga do VD.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> O mecanismo de ação do BIA é a contrapulsação aórtica, a elevação da pressão diastólica na raiz da aorta, a redução da pós-carga e o consequente incremento no DC.<sup><xref ref-type="bibr" rid="B7">7</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup></p>
				<p>O uso de suporte circulatório mecânico deve ser considerado para pacientes com doenças potencialmente reversíveis e HAP farmacologicamente irreversível. A International Society for Heart and Lung Transplantation (ISHLT) recomenda como classe IIB o uso de suporte circulatório mecânico no manejo de pacientes com HAP.<sup><xref ref-type="bibr" rid="B6">6</xref></sup></p>
				<p>O estudo ESCAPE (<italic>Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness</italic>) assinalou eventos adversos associados ao implante do CAP como arritmias, septicemia, perfuração ou ruptura da artéria pulmonar e até morte. Diante disso, concluiu-se que os riscos superariam os benefícios do seu implante, estimulando diversas diretrizes a não indicarem a cateterização de artéria pulmonar.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> Apesar do risco, o uso cauteloso associado a técnicas de minimização de riscos torna sua utilização mais segura, auxiliando na otimização do suporte do paciente, como ocorreu no caso em questão.</p>
			</sec>
			<sec sec-type="conclusions">
				<title>Conclusão</title>
				<p>A IC em seus estágios avançados apresenta-se em cenários desafiadores do ponto de vista terapêutico e de definição de terapia de destino. A HAP constitui um marcador da IC avançada, e o uso da monitorização invasiva pode ser útil em relação à otimização terapêutica à beira do leito e à adequação de parâmetros hemodinâmicos permissivos ao TC.</p>
			</sec>
		</body>
		<back>
			<fn-group>
				<fn fn-type="supported-by" id="fn4">
					<p><bold>Fontes de financiamento</bold></p>
					<p>O presente estudo não teve fontes de financiamento externas.</p>
				</fn>
				<fn fn-type="other" id="fn5">
					<p><bold>Vinculação acadêmica</bold></p>
					<p>Não há vinculação deste estudo a programas de pós-graduação.</p>
				</fn>
				<fn fn-type="other" id="fn6">
					<p><bold>Aprovação ética e consentimento informado</bold></p>
					<p>Este artigo não contém estudos com humanos ou animais realizados por nenhum dos autores.</p>
				</fn>
			</fn-group>
		</back>
	</sub-article>
</article>